The thermal environment in chicken housing is a primary determinant of production performance and efficiency (Purswell et al., 2012). Exposure of chickens to chronic environmental temperatures (high or low) during the period of production may have an adverse effect on growth performance, meat yield, immune response, and mortality (Washburn, 1985; Howlider and Rose, 1989). A high ambient temperature increases chickens' energy requirement and results in significant losses from a less efficient conversion of feed to meat or egg, which detrimentally impacts the health and productivity of chickens. Thermal stress incites a classic family of molecular chaperones known as heat shock proteins (HSPs) which play protective roles against tissue damage (Calderwood, 2010).

Feed restriction has been identified as one of the causes of physiological stress in chickens (Najafi et al., 2015), especially in young birds because they are in rapid growth stages and have high metabolic requirements (Mench, 2002). Most times, feed restriction is initiated during the first 3 weeks of age (Soleimani et al., 2012; Trocino et al., 2015) and can induce stress, as indicated by elevated corticosterone concentrations, enhanced abnormal behaviors, and impaired welfare and health of chickens (Yan et al., 2021). Feed deprivation can be applied in different ways either quantitative or qualitative. The reduction in the amount of the feeds is known as quantitative feed restriction while decreasing the energy content in a given feed is known as qualitative feed restriction (Urdaneta-Rincon and Leeson, 2002). Feed restriction has been previously reported to reduce body weight gain, body weight, feed consumption, and meat quality (Urdaneta-Rincon and Leeson, 2002; Abu-Dieyeh, 2006; Cornejo et al., 2007; Hassanabadi, 2008; Boostani et al., 2010; Azis and Afriani, 2017). The negative effect of feed restriction in chickens might depend on the extent, timing, and intensity (Trocino et al., 2020). Chicks subjected to 95, 90, or 85% feed restriction from 5 to 42 d of age had lowered body weights compared to the ad libitum fed group. Broilers challenged with qualitative feed restriction (fed mash only) from 1 to 7 wk had reduced breast meat yield at 42 and 49 d (Urdaneta-Rincon and Leeson, 2002). Gratta et al. (2019) observed that early and late feed restriction (80%) from 13 to 22 d of age and 23 to 37 d of age impaired the growth performance of broiler chickens. An experiment conducted by Hassanabi and Moghaddam (2006), showed that restricted group of birds fed a mixture of 50:50 rice hulls, with the supplementation of trace minerals and vitamins from 4 to 11 d of age had reduced serum thyroxin and average final body weight on d 11 compared with ad libitum fed group, but was compensated on d 42 of age. Similary, growth performance parameters such as feed intake and body weight were significantly reduced in 3 to 5 d old birds when fed 8 hours per day from 7 to 21, 14 to 28, 21 to 35 d of age than those in ad libitum group (Boostani et al., 2010). Carcass weight, breast weight and yield of broilers were significantly decreased in restricted birds from 7 to 21 d of age, which confirm the adverse effects of eary restriction on meat quality (Boostani et al., 2010). Englmaierová et al. (2021) showed that the reduction in diet level (20% and 30%) from 29 to 57 d of age negatively affected the dressing percentage and breast yield while the leg yield and muscle fibers increased with increasing restriction levels in cockrels.

Feed-restricted broilers may result in high levels of plasma corticosterone as a stress indicator (Soleimani et al., 2012; Najafi et al., 2018). Janczak et al. (2007) reported that feed restriction increased the plasma and fecal corticosterone in birds. There is also a possibility of corticosterone transfer from stressed layer hens into their eggs, thus altering the growth and welfare of chicks (Janczak et al., 2007). Najafi et al. (2015) noted a significant linear relationship between plasma circulating corticosterone, H/L ratio, dopamine concentrations, and feed restriction. Aside establishing feed restriction as a chronic stress inducer, Yan et al. (2021) observed alteration in the gut microbiota composition in response to severe feed restriction. Hangalapura et al. (2005) revealed that severe feed restriction promoted reactive oxygen intermediates and decreased the relative weight of immune organs (spleen and bursa). Other stress behaviors associated with feed restrictions include object pecking, increased sitting, lying, decreased standing and feeding, and increased H/L ratio, which impeded growth rate and immune functions (Sandilands et al., 2005; Bowling et al., 2018; Trocino et al., 2020).

There is extensive evidence that feed restriction can result in physiological stress responses (De Jong et al., 2002; Janczak et al., 2007). De Jong et al. (2002) observed an increased in body temperature and a clear repeated sound in the heart rate of feed-restricted birds, whereas such a rhythm was blunted in ad libitum-fed birds. Feed-restricted broilers beyond 4 days had lowered counts of red blood cells, hemoglobin, and mean cell heamoglobin concentration compared to birds fed ad libitum (Bratte, 2011). Feed restriction decreased thyroid hormone triiodothyronine, thyroxine, and albumin in broiler chickens (Azis et al., 2012). Yang et al. (2010) reported a decrease in SOD activity, swollen mitochondria, and reduced cristae liver in feed-restricted groups, which may affect lipid metabolism in chickens. In addition, feed restriction significantly altered glucose, albumin, chlorine, ALT, and cholesterol in birds (Demir et al., 2004). Activities of jejunal alkaline phosphatase and pancreatic trypsin, amylase, and lipase were reduced significantly in response to feed restriction (Palo et al., 1995). Significant changes of blood biochemical indices caused by feed restriction implies that feed restriction poses a serious stress on chickens during the growth period (Rajman et al., 2006).

Stocking density (SD) is a critical environmental factor, identified as one of the causes of physiological stress among poultry species which has become a widespread concern (Li X. M. et al., 2019). SD has serious implications for the broiler industry because profits can be maximized as the number of birds per unit area increases. It is possible that assigned SD are focused on profit maximization at the expense of chickens' health (Estevez, 2007). SD directly influences the health, welfare, and performance of birds. With the rapid growth rate of present-day broilers, high SD is highly associated with leg deformities such as footpad dermatitis, lameness, hock burns, and abnormal gaits (Bilal et al., 2021). In layers, high SD has been confirmed to increase eggshell lightness, broken eggs, reduced laying rates, shell color, strength, thickness, and relative weight (Wang et al., 2020). Previous studies have reported that SD stress can affect the performance and behavior of chickens (Eugen et al., 2019; Li W. et al., 2019). Behaviors such as increased anxiety (Li W. et al., 2019), fearfulness (Eugen et al., 2019), cannibalism (Turkyilmaz, 2006), decreased locomotion, ground pecking and preening patterns (Hall, 2001), decreased feed intake, walking and drinking (Ibrahim et al., 2018), increased resting (Son, 2013) are associated with high SD. On growth performance, increasing SD above 30 kg of BW/m² negatively affected live performance (Dozier et al., 2006) growth rate, feed consumption, and feed conversion of chickens at 28 d of age (Dozier et al., 2006). Another study concluded that increasing the SD rate from 28 to 40 kg of BW/m² had negative effects on the performance and welfare of broiler chickens (Abudabos et al., 2013). High density stocked birds had lower body weight and high levels of plasma corticosterone which indicated stress and impaired welfare in birds (Eugen et al., 2019). Tong et al. (2012) observed a linear decrease in individual body weight and feed intake with increasing SD from 1to 28 d of age in a local chicken breed. On the contrary, body weight increased with increasing SD in chickens raised from d 1 to 10 as reported by Guardia et al. (2011). The findings of Guardia et al. (2011) showed that broilers' body weight was not affected by SD from d 10 to 24 and d 24 to 32; however, from d 32 to 39, high SD adversely affected broilers' body weight and feed conversion ratio. More findings on broilers affirmed that high SD decreased body weight and overall performance during the grower and finisher phases (Magnuson et al., 2020).

Moreover, SD significantly affects physiological stress indicators of broiler chicks. As SD increased, stronger stress responses were seen, including poor performance (Qaid et al., 2016). High SD was associated with decreased locomotor activity and increased H/L ratio, bursa weight, and oxidative stress (Simitzis et al., 2012). Another evidence showed that heterophils, H/L ratio, and serum corticosterone were greater in birds stocked at 10 birds/m² than in those stocked at 6–7 birds/m² (Kang et al., 2016). Elevation of hemoglobin was clearly seen in the high-density-stocked group due to overcrowding stress. Less oxygen is supplied when birds are overcrowded, leading to hypoxia, a stimulus for erythropoietin production, resulting in erythropoiesis in stressed chickens (Lokhande et al., 2009). Previous literature showed a positive correlation between SD and physiological stress response (i.e., stress indicators) (Bozkurt et al., 2008). High SD challenged hens experienced a significant increase in plasma insulin and glucose levels (Mirfendereski and Jahanian, 2015). Lallo et al. (2012) observed that plasma protein and rectal temperature increased with increasing SD. Blood biochemical parameters such as Ca, phosphorus (P), potassium (K), blood glucose and AST were found to decrease with increasing SD (Pandurang et al., 2011; Lallo et al., 2012; Mirfendereski and Jahanian, 2015). Özbey (2007) also established that SD can affect blood biochemical indices and antibody titers. Chegini et al. (2018) specified that plasma immunoglobulins, corticosterone, and nitric oxide concentrations were higher in chickens stocked at a high density compared to those at normal density. It has been previously studied by Cengiz et al. (2015) that SD stress can activate the HPA axis in the affected birds and thereafter increase corticosterone, prompting the release of pro-inflammatory cytokines. Elevated SD from 28 to 40 kg BW/m² stimulated a state of hemodilution and a decrease in packed cell volume (PCV) in broiler chickens (Abudabos et al., 2013).

High SD has also been reported to affect carcass traits and meat quality (Li W. et al., 2019). Broiler chickens stocked at a high density had significantly reduced breast muscle yield, tibial length, tibial width, and tibial weight. Elevated SD decreased breast filet weight and its relative yield and breast tender weight (Dozier et al., 2006). High density stocked birds had reduced tibia quality compared to low-density stocked ones (Wang et al., 2020). In addition, Wang et al. (2014) observed a reduction in drip loss of broilers breast muscle, triggered by high SD, while Pekel et al. (2020) reported that the length of breast filet was significantly increased among stressed broilers. Drip loss can show quality deviations as the volume of drip loss is an indicator of oxidative stress in muscles (Wang et al., 2014). Other recent findings showed high drip loss and breast muscle redness shortly after slaughter in the high SD birds compared to other treatments groups (Wu et al., 2020). Bilgili and Hess (1995) observed that carcass quality was reduced in female chickens subjected to SD stress while breast filet yield was reduced in male chickens. The mRNA expression level of myostatin, a protein involved in the regulation of fat mass hens was increased with increasing SD in broiler breeder hens (Li X. M. et al., 2019). Conversely, some previous studies have revealed that SD stress did not affect meat quality or carcass traits in chickens (Simitzis et al., 2012; Tong et al., 2012; Goo et al., 2019). Variation in results might be due to differences in production systems.

Chickens stocked at high densities may be susceptible to severe oxidative stress (Simitzis et al., 2012; Wu et al., 2018). Metabolic alterations resulting from SD stress can cause excessive production of ROS that leads to oxidative damage of biomolecules (Fang et al., 2002). Antioxidant enzymes such as SOD, catalase (CAT), glutathione reductase and glutathione peroxidases (Gpx) utilize synergistic actions in scavenging free radicals and ROS (Fang et al., 2002). Elevated SD increased malondialdehyde (MDA) significantly while the SOD and CAT activity remained unaffected (Jobe et al., 2019). As reported by Simsek et al. (2009), high SD increased serum MDA level and reduced GSH-Px but did not change serum CAT and GSH levels. A current study found that high SD significantly decreased total antioxidant capacity, GPx activity and increased plasma MDA (Miao et al., 2021). High SD elevated glutathione concentration in the plasma, breast, and thigh of growers but decreased it in the liver and thigh of the finishers (Magnuson et al., 2020). The detailed characteristics of the included studies on SD are summarized in Table 3.

Environmental pollutants such as Arsenic (As), copper (Cu), ammonia (NH₃), hydrogen sulfide (H₂S) can induce oxidative stress when inhaled by chickens (Hu et al., 2018; Wang et al., 2018; Xing et al., 2019). These pollutants can inhibit antioxidant enzymes like CAT and GPx (Sawyer et al., 2002). Wang et al. (2018) reported that exposure to As and Cu provoked an imbalanced oxidant status in the intestines of chickens which may impair the functioning of the GIT (Wang et al., 2018). Higher MDA and hydroxyl radical content and reduced CAT and GPx were seen in chickens exposed to Cu and As, which affirmed the occurrence of lipid peroxidation of the heavy metals and a close connection with oxidative stress (Zhao et al., 2018). Similarly, Nie et al. (2020) observed that As and Cu could prompt redox imbalance in the chicken brain, accompanied by apoptosis in brain cells and neurological damage. Other negative effects of As and Cu were alteration of the inflammatory and immune-regulated cytokines, causing toxicity in the chicken thymus (Liu et al., 2018). While Cu is needed for several cellular processes and enzymes in the organisms, an excess amount produces cellular damage leading to several adverse effects and diseases (Öhrvik et al., 2017). Experimental studies suggested that exposure of chickens to excessive Cu triggered oxidative stress.

Ammonia (NH₃) is one of the environment pollutants of greatest concern and its emissions play a vital role in the formation of secondary inorganic aerosols (Artíñano et al., 2018). The rise in NH₃ concentrations depends on the housing systems. Concentrations of NH₃ are usually higher in aviaries and floor systems because manure is not regularly removed compared to furnished cages systems (David et al., 2015). Evidence showed that an upsurge of NH₃ could adversely affect the health, behavior, and performance of chickens, and can predispose them to respiratory infections and pathogens (Yahav, 2004; David et al., 2015). An increase in NH₃ levels triggered inflammation in broiler chickens' respiratory tracts. 15 ppm NH₃ altered tracheal microbiota composition that led to the tracheal injury, enhancing their susceptibility to pathogens (Zhou Y. et al., 2021). Wang et al. (2019a) found that NH3 exposure could cause oxidative stress, intestinal inflammation and disrupt the chicken intestine integrity. Previous findings have shown that a high concentration of NH₃ increased serum biochemical indices such as AST, ALT, AKP, GGT, CK and ALB in chickens, which signified a negative effect on the immune organs (Lu et al., 2017; Shah et al., 2020). Liu et al. (2020) indicated that exposure of chickens to a high concentration of NH₃ disrupted the ecological balance of the lung tissue flora, increased some pathogenic bacteria such as Escherichia/Shigella and damaged their lung tissue.

Hydrogen sulfide has been widely researched as an environmental stressor that causes respiratory and immune damage in chickens (Li X. et al., 2020; Yin et al., 2020; Song et al., 2021). Results showed that increasing H₂S concentrations decreased cell viability, and differentially inhibited neutrophil viability and neutrophil extracellular trap (NET) (Yin et al., 2020). Neutrophils perform immunity roles through the formation of NET (Selders et al., 2017). H₂S damaged broiler chicken's trachea by dysregulating necroptosis and apoptosis (Li X. et al., 2020). A previous study revealed that H₂S induced oxidative stress in the chicken trachea, indicated by increased levels of hydrogen peroxide (H₂O₂) and MDA, and decreased SOD, GSH, and CAT activity, which resulted in inflammatory injury mediated by FOS/IL8 signaling (Chen et al., 2019). Likewise, H₂S decreased CAT and total antioxidant capacity (T-AOC) activities and increased H₂O₂ and nitric oxide content in broilers' myocardial region and in the bursa (Hu et al., 2018; Wang et al., 2019b). Chi et al. (2018) suggested that H₂S triggers inflammatory responses and oxidative stress by enhancing ROS production, then impairing energy metabolism and immune system in the chickens. Aside from cellular and oxidative damage, concentrated H₂S negatively affects growth performance parameters such as average daily gain and body weight, the carcass yield, and increased water loss rate of breast and leg (Wang et al., 2011).

Vitamin A is a fat- for bone health and development soluble vitamin, which when added to the diet, is converted to retinoid within the intestine, liver, and other tissues (Huang et al., 2018). Vitamin A is obtained from plant diets as provitamin A carotenoids while from animal sources as retinoids. Forms of provitamin A carotenoids includes α-carotene, β-carotene and βcryptoxanthin (Maqbool et al., 2018). Emerging literature reported that vitamin A is involved in the development of the immune system and plays an essential role in cellular and humoral immune response (Aydelotte, 1963). Vitamin A is involved in the proliferation and differentiation of epithelial cells (Thomas et al., 2005). Vitamin A has been established to enhance normal intestinal barrier function, regulates the composition of the intestinal bacteria and subsequently helps in maintaining innate immunity and gut integrity in humans (Quadro et al., 2000; Thurnham et al., 2000). Pang et al. (2021) showed that the dietary supplementation of Vitamin A significantly changed the gut microbiota and ameliorated a chronic gastrointestinal tract inflammation know as Ulcerative colitis in mice. Supplementation of Vitamin A promoted the restoration of the damaged small intestine in rats (Xia et al., 2019) while Vitamin A deficiency altered Bacteriodes/Firmicutes ratio, and decreased rates of short chain fatty acid (Tian et al., 2018).

In poultry diets, the importance of vitamin A has been given wide attention because of production losses associated with vitamin A deficiencies, including growth dysfunction, weakness, ruffled feathers, decreased egg production, and immune depression (Sklan et al., 1994; Shojadoost et al., 2021). Vitamin A insufficiency often leads to serious infection, through substitution of many secretory epithelia cells with non-secretory ones (Aydelotte, 1963). Depression of the chick antibody production and proliferative responses of T lymphocytes have been associated with lack of Vitamin A in the chicks diet (Sklan et al., 1994). Vitamin A deficiency was also associated with the significant reduction in ovarian stroma and follicles weights (Chen et al., 2016). On the other hand, previous works have established that excessive Vitamin A has adverse effects on chicken health (March et al., 1972; Lessard et al., 1997). Excessive or insufficient vitamin A increased vulnerability of the chicks to Eschericia coli infection, followed by depressed immune responses (Friedman et al., 1991). Yuan et al. (2014) observed that the addition of vitamin A at 135,000 IU/kg differentially decreased peripheral blood T-cell production at week 24, adversely affected the liver function and reproductive performance in broilers breeders. Similarly, Sklan et al. (1994) revealed that the supplementation of Vitamin A above 6,000 IU/kg negavely affected the immune system of broilers.

The roles of vitamin A have been studied in heat-stressed chickens (Lin et al., 2002; Kucuk et al., 2003) but sparsely studied in other types of environmental stress. Vitamin A has been supplemented in HS challenged birds and found to be beneficial in terms of laying performance and immune function in layer chickens (Lin et al., 2002). Lin et al. (2002) found that high level of vitamin A supplementation (9,000 IU/kg) improved the feed intake and laying rate of heat-stressed hens compared to the control group (3,000 IU/kg). Likewise, Abd El-Hack et al. (2019) observed that Vitamin A addition at 8,000 IU/kg significantly increased the feed intake and feed conversion ratio of layers raised under high temperature. Dietary supplementation of vitamin A in combination with zinc has been suggested as an effective way of managing heat-stress-related production depression in broilers (Kucuk et al., 2003).

It is required to supplement B vitamins in chickens' meal to ensure maximum production potential. Different forms of vitamin B such as riboflavin, pantothenic acid, folate, B12 and niacin improved production performance of chickens fed with low density diet (Suckeveris et al., 2020). Vitamin B1 (thiamine) can be classified as part of the anti-stress vitamins due to its strong antioxidant ability (Lukienko et al., 2000). Miladinović et al. (2021) affirmed the antioxidant and anti-inflammatory properties of vitamin B1 in quail brains treated with organophosphate pesticides. Vitamin B1 deficiency caused neurological damage and severe cardiovascular infection because of excessive production of ROS in the brain (Miladinović et al., 2021). Thiamine plays a key role in glucose metabolism and functioning of the tissue, organ, and body (Kerns et al., 2015). Owing to its multidimensional roles in biochemical reactions, thiamine is essential for body growth and development (Lonsdale, 2019). Vitamin B3 (niacin) helps in the prevention of metabolic diseases in animals. Supplementation of 6–12 g niacin has been established to defend dairy cattle from chronic HS (Panda et al., 2017). Niacin is an essential nutrient needed by the body for proper metabolism and digestion, and also support blood circulation and the brain (Moneva et al., 2008). Riboflavin is involved in the reduction of oxidized glutathione and its deficiency led to an increase in lipid peroxidation and a decrease in antioxidant ability (Saedisomeolia and Ashoori, 2018). Previous studies have confirmed riboflavin as a strong antioxidant that protect the body against oxidative stress (Wang et al., 2014). Kumar et al. (2020) showed that a combination of riboflavin and selenium nanoparticles can alleviate high temperature effects and arsenic pollution in fish. An additional study revealed that riboflavin lessens oxidative stress and tissue damage in diabetic mice (Alam et al., 2015). Many studies involved the in ovo feeding of vitamin B in chickens (Momeneh and Torki, 2018; Teymouri et al., 2019). Teymouri et al. (2019) suggested that in ovo feeding of the vitamin B12 positively influenced the performance of broiler chickens. Momeneh and Torki (2018) recorded that in ovo injection of vitamin B6 and B12 ameliorated the ethanol induced oxidative stress in chicken embryos.

Another type of vitamin B known as folate (vitamin B9), is an essential component of an healthy diet, known to improve cardiovascular diseases through its homocysteine lowering potential and necessary for normal body functioning (Nakano et al., 2001; Patel and Sobczyńska-Malefora, 2016). Folic acid is the synthetic form of folate and is supplemented in diets to increase folate levels (Powers, 2007). It exhibits similar antioxidant effect as vitamin C and E (Gursu et al., 2004; Sinbad et al., 2019). Gouda et al. (2020) stated that the dietary supplementation of the combination of folic acid and vitamin C (1.5 mg/kg) significantly improved the growth performance, immune status, blood biochemistry parameters, and antioxidant capacity of broilers raised under HS conditions. In quail, dietary supplementation of folic acid (2 mg/kg) alleviated the negative effects of CS on growth performance, lipid peroxidation, and serum concentrations of homocysteine (Sahin et al., 2003a). In mouse, administration of folic acid ameliorated the inhibitory effects of HS on the pre-implantation embryos development (Koyama et al., 2012), served a protective role by reducing the CAT, SOD, and glucose level (Padmanabhan et al., 2018; Mutavdzin et al., 2019). The ameliorative effects of vitamin B in chickens challenged with environmental stress are rarely studied. Given the importance of vitamin B, it may be worthwhile to supplement chickens' diet with vitamin B especially during stress conditions.

Vitamin C is an alternative functional nutrient adopted for stress amelioration in farm animals because of its antioxidant ability. Vitamin C is water-soluble in form. It prevents cells from oxidative damage and improves cell immune function (Buettner, 1993; Chambial et al., 2013). Under normal conditions, poultry synthesizes sufficient vitamin C needed to meet physiological needs; however with HS exposure, vitamin C requirement increases and the body's capacity becomes inadequate (Attia et al., 2016). Thus, it is recommended that under stressful conditions, poultry diets should be supplemented with vitamin C to augment the body's synthesis. Several studies have investigated the effect of vitamin C supplementation in chickens challenged with HS. Attia et al. (2009) showed that vitamin C supplementation improves the humoral immune response and eradicates the negative effects of HS on broiler chickens. Supplementation of vitamin C also improved growth performance in heat-stressed broiler chickens under standard animal density conditions (Saiz del Barrio et al., 2020). In a study conducted by Ferket and Qureshi (1992) on the efficacy of different vitamins and electrolyte treatments in drinking water for heat-stressed broilers, the authors observed that vitamin C treatment increased body weight gain and feed conversion by 3 and 5%, respectively and reduced the rate of HS induced death by 63%. In addition, dietary vitamin C supplementation for HS-challenged broiler chicks positively affected the relative weights and immune status of bursa, thymus, and spleen (Naseem et al., 2005). Also, supplementation of vitamin C at 200 ppm was shown to be beneficial for improving weight gains, nutrient digestibility, carcass traits, and bone resistance and helped to reach the full genetic potential of commercial broilers (Lohakare et al., 2005). Similarly, Abidin and Khatoon (2013) found that vitamin C ameliorated heat stress-induced complications such as infertility, poor semen quality, poor immunity, and mortality in birds. Related functions have been observed in vitamins C and E; both positively affected the immune system by improving the production of antibody, macrophage activity, and humoral immunity in chickens. It is proposed that the combination of vitamins C and E in broiler chicken diets might improve their immune system functions and performance (Shakeri et al., 2020).

Furthermore, results revealed that vitamin C alleviated the adverse effects of CS and HS in poultry performance by decreasing synthesis and secretion of corticosteroids (McDowell, 1989; Kutlu and Forbes, 1993). A previous study observed that the combination of 250 mg vitamin C and 400 μg chromium per kg of diet prevented rise in blood glucose, total cholesterol induced by CS (Khukhodziinai et al., 2021). Similar diet administered by Khukhodziinai et al. (2021) resulted in optimum performance in layers challenged with CS (Sahin and Sahin, 2001). Rajabi and Torki (2021) found that the dietary supplementation of 240 mg/kg vitamin C and zinc improved the egg quality of layers challenged with cold temperature between 13 and 15°C. Sahin and Sahin (2001) concluded that the depressive effect of CS in chickens can be alleviated by vitamin C and chromium. Inconsistent findings have also been reported on the modulatory roles of vitamin C in chickens subjected to high SD (Jahanian and Mirfendereski, 2015; Shewita et al., 2019). Jahanian and Mirfendereski (2015) found that 500 mg/kg vitamin C supplementation had no significant effect on the growth performance of broiler chickens subjected to high SD but decreased plasma and yolk MDA. A recent study by Yu et al. (2021) observed that 200 mg/kg had no marked effects on the growth performance, meat quality, and intestinal permeability of broiler chickens stocked at high density (12 birds/m²). Shewita et al. (2019) reported that 200 mg/kg vitamin C improved final body weight, feed intake and decreased mortality in broilers reared in high SD (15 birds/m²). The inconsistency in the findings might be attributed to the strain of the animal or different SD used (Yu et al., 2021). Vitamin C was also reported to decrease plasma corticosterone caused by high SD in broilers (Mirfendereski and Jahanian, 2015). Vitamin C could ameliorate the negative effects of environmental stress by increasing the antioxidant ability of the birds (Jahanian and Mirfendereski, 2015; Zangeneh et al., 2020).

Vitamin D is a fat-soluble vitamin that is gotten by either exposing the skin to sunlight or by dietary supplementation (Lamberg-Allardt, 2006). Vitamin D is available in animal-derived (vitamin D3, cholecalciferol) and plant-derived (vitamin D2, ergocalciferol) forms (Jones, 2018). It is transported in the blood by the vitamin D binding protein into the liver for hydroxylation to 25-hydroxyvitamin D3 (25(OH)D3), which can then be converted to its active metabolite 1,25(OH)2D in numerous cell types (Christakos et al., 2010). Vitamin D plays a role in the maintenance of Ca and P for bone health and development (Lamberg-Allardt, 2006). Also, it is involved in sustaining normal immune function and mediates between innate and adaptive immunity by influencing vitamin D receptors (VDR) (Li et al., 2014). Vitamin D can impact the gut function by binding to its VDR and maintain the epithelia integrity of the organism (Fakhoury et al., 2020). Vitamin D has been confirmed as a prohormone due to its involvement in the physiology of stressed birds (Huff et al., 2000). The addition of vitamin D in turkey diets improved their body weight, disease resistance, and white blood cell counts despite being challenged with dexamethasone (DEX) and Escherichia coli repeatedly (Huff et al., 2000). In mice, vitamin D₃ alleviated oxidative stress induced by lipopolysaccharide challenge through regulation of antioxidant and oxidant exymes gene (Xu et al., 2015). Geng et al. (2018) also affirmed that vitamin D₃ supplementation protected laying hens against immunological stress caused by Escherichia coli lipopolysaccharide challenge. A recent study revealed that dietary supplementation of an active metabolite of Vitamin D3 for layer chickens reversed the effect of high SD on T-AOC, MDA content, and antioxidative catalase activity (Wang et al., 2021). Additional evidence suggests that dietary vitamin D is effective in reducing the severity of lameness caused by environmental stress through tibial dyschondroplasia reduction (Nääs et al., 2012). Vitamin D supplementation promotes gene expression related to antioxidation and serves as therapy in cold-related cases (Lei et al., 2017). Other studies have established the antioxidant and anti-inflammatory roles of vitamin D in rat (Manna et al., 2017; El-Boshy et al., 2019). No study has recorded the protective roles of vitamin D in chickens challenged with different forms of environmental stress.

Vitamin E is a chain-breaking antioxidant that protects the membranes of cells from being scavenged by lipid peroxyl radicals (Gao et al., 2010). Supplementation of vitamin E in chicken diets is necessary because they cannot synthesize vitamin E on their own under normal and stress conditions (Shakeri et al., 2020). Vitamin E supplementation can enhance immune system and decrease influence of corticosterone induced by stress, aside protecting cells against oxidative damage (Attia et al., 2016). Min et al. (2018) found that dietary supplementation with vitamin E increased body weight and GSH-Px mRNA expression of breeder roosters challenged by oxidative stress when compared to the control treatment, suggesting that vitamin E could improve antioxidant ability and immune performance in oxidative-stressed chickens (Min et al., 2018). An additional study indicated that vitamin E supplementation improved the performance of broiler chickens by alleviating the oxidative stress induced by DEX treatment (Singh et al., 2006). Aside from growth performance, the effectiveness of vitamin E as an anti-stress substance has also been proven by Niu et al. (2009) who reported that heat-stressed broiler chickens had improved immune response when fed with vitamin E supplemented diets (Niu et al., 2009). A different study affirmed that vitamin E helps in promoting humoral immune response which may influence the growth of lymphoid cells and immunocompetence of chicks (Surai et al., 2019). In layers, Puthpongsiriporn et al. (2001) reported that dietary supplementation of vitamin E at 65 IU/kg diet enhanced higher egg mass, egg quality, and egg yolk formation during HS. Further results revealed that lipid peroxidation in yolk and plasma resulting from HS can be ameliorated with 65 IU/kg of vitamin E supplementation (Puthpongsiriporn et al., 2001). Research on breeders and cockrels indicated that an increase in vitamin E supplementation in animal diet increased resistance to various forms of stress (Qureshi et al., 2018). A previous report concluded that dietary supplementation of 250 mg vitamin E/kg of diet provided during and after HS is effective for alleviating, the symptoms and adverse effects of chronic HS in chickens (Bollengier-Lee et al., 1999).

In addition, vitamin E supplementation in the diet of broilers exposed to CS caused a significant reduction in ascites-related mortality (Akşit et al., 2008; Qureshi et al., 2020). Increase in antibody production was observed in broiler chickens challenged with extreme cold stress (5 ± 2°C) after vitamins fortification (Sandhu et al., 2013). Qureshi et al. (2020) found that the intestinal health of broiler chickens subjected to CS was improved with the addition of 250 mg/kg vitamin E in their diet. Correspondingly, pathological changes on the chicken intestine (duodenum, jejunum and ileum) induced by oxidative stress in response to virus infection were fully alleviated by addition of vitamin E (Rehman et al., 2018). Birds fed vitamin E had a significantly lower LPS-induced inflammatory response, as indicated by lower IL6 RNA expression levels, suggesting a protective effect from natural-type vitamin E when a chicken encounters a bacterial component (Kaiser et al., 2012). The roles of dietary supplementation of vitamin E in ameliorating the negative effects of SD in chickens have been studied. 200 mg/kg vitamin E diet improved the growth performance, liver functions, and decrease the pathogen counts in broilers stocked at high density (Desoky, 2018). Selvam et al. (2017) reported that vitamin E positively influenced the body weight, feed conversion ratio, liver GSH, and MDA levels of broiler chickens reared under high SD. In a study conducted by El-Gogary et al. (2015), vitamin E protected the lymphoid organs such as spleen, bursa, thymus from the negative effects of high SD by enhancing the organs to produce more lymphocytes that aided in improving the birds immunity. The positive effects of dietary vitamin supplementation in chickens challenged with different forms of environmental stress are summarized in Table 4.