Selenium’s Role in Optimizing Poultry Nutrition - Glamac

Selenium’s Role in Optimizing Poultry Nutrition

Selenium, discovered in 1817 by J.J. Berzelius, initially attracted interest from diverse industries like glassmaking, pottery, and electronics. However, it was not until around the 1930s that studies on selenosis sparked curiosity in its biological activity. By the 1950s, research intensified, particularly focusing on its preventive effects against liver necrosis, exudative hemorrhagic diathesis, and muscle dystrophy, as well as its relationship with vitamin E.

Selenium in the diet exists in inorganic or organic forms. Factors influencing its availability include methionine, thiols, heavy metals, and vitamin C (Fairweather-Tait and Hurrell, 1996). Absorption, retention, and metabolism depend on intake and chemical form, with the duodenum showing the highest absorption rates (Wright and Bell, 1966). Organic forms, like Se-methionine, are absorbed more efficiently, primarily in the small intestine, and are excreted through the kidneys. Se is transported in the bloodstream bound to plasma proteins and distributed to tissues (Cousins and Cairney, 1961). Tissue deposition is largely labile.

Intestinal absorption of Se is greater in monogastric animals compared to ruminants. Excreted amounts vary based on Se intake, compound type, diet composition, and animal species (Suchý Pet al. 2014). Se is eliminated through urine, feces, and expired air, serving as a detoxification route with high dietary intake. Ruminants primarily excrete Se via feces, while monogastric animals excrete more through urine. Se, a trace element, plays vital biological roles across various organisms, including humans, with effects being dose-dependent, essential at low levels, and toxic at higher concentrations (Umysovaet al., 2009). Surai and Fisinin (2014) conducted an extensive study on Se in poultry breeder nutrition.

Sources of Selenium and Their Efficiency

Poor Resorption

  • Stable
  • Biologically inactive
  • Poor Resorption

Inorganic Selenium compounds

  • Sodium Selenite
  • Mildly biologically active
  • Accelerates oxidation process (detrimental to health)

Organic Selenium compounds

  • Se-Met and selenocysteine (Se-Cys), are integral parts of proteins.
  • Most Active
  • Se-Met is plant based while Se-Cys is of animal origin

Other Selenium enriched feedstuff

  • Scenedesmus quadricauda (selenium-enriched Scenedesmus biomass)
  • Se-enriched unicellular alga Chlorella
  • Se-enriched Yeast

It should be noted that activity of glutathione peroxidase (GSH-Px) in the serum remains the same both in the organic and the inorganic form.Maximum activity of GSH-Px is already achieved at the Se level of 0.1 mg/kg of fodder in the case of both organic and inorganic form. This activity is independent of the chemical form (Xia et al. 1992).

De Almeida et al. (2012) investigated the impact of dietary supplementation with chelated selenium on broiler chicken meat quality. They found that incorporating chelated selenium into the feed improved meat quality by reducing lipid oxidation and cooking loss. However, it did not lead to an increase in glutathione peroxidase (GSH-Px) activity.


Nanotechnology has introduced innovative products like nano-selenium (nano-Se) into the realm of nutritional supplements, offering increased chemical reactivity. However, this heightened reactivity raises concerns about potential toxicity. Cai et al. (2012) investigated the effects of nano-Se on broiler chickens, noting significant impacts on yield, meat quality, immune functions, oxidation resistance, and tissue selenium levels. Similarly, Zhang et al. (2001) studied nano-red elemental selenium (nano-Se) in mice and rats, finding lower acute toxicity compared to sodium selenite and comparable effects on tissue selenium levels and glutathione peroxidase activity. Nano-Se displayed less pro-oxidative effects than selenite, demonstrating similar bioavailability and antioxidant properties. Selenium, facilitated by specific enzymes, plays vital roles in antioxidant protection, immune function, thyroid health, reproductive function, and disease prevention, including cardiovascular diseases and various carcinomas.

Selenium and meat and egg quality

Selenium levels in meat and animal products exhibit seasonal fluctuations and are influenced by ration composition. Supplementing broiler diets with selenium and vitamin E improves oxidative stability under heat stress, while organic selenium enhances meat quality by increasing red color intensity and reducing drip losses. Additionally, selenium supplementation leads to reduced lipid oxidation and cooking loss in meat, linearly reduces abdominal fat, and improves pH levels, water retention, and shear force, enhancing overall meat quality. Studies show that both sodium selenite and selenium-enriched yeast increase glutathione peroxidase activity and oxidative stability in meat, with added benefits from vitamin C supplementation, including increased protein concentrations and reduced lipid oxidation during storage.

Skrivan et al. (2010b) examined the levels of selenium (Se) and α-tocopherol in eggs of egg-laying hens fed diets enriched with Se-Met, sodium selenite, and vitamin E. Both forms of Se supplementation significantly increased Se concentration in egg yolks and whites, with Se-Met showing a more pronounced effect. Se-Met supplementation also increased α-tocopherol content and moderately reduced yolk cholesterol. Skrivan et al. (2013) found that supplementation with sodium selenite or Se-enriched yeast improved laying performance, while vitamin C supplementation decreased feed intake and egg production. Selenite and Se-enriched yeast increased vitamin E concentration in yolks, Se concentration in yolks and albumen, and improved yolk lipid oxidative stability. Attia et al. (2010) observed that Se supplementation increased egg weight, egg mass, and improved feed conversion ratio, with significant reductions in plasma cholesterol concentration. Additionally, Kralik et al. (2009) found that Se concentration in diets significantly influenced Se content in albumen and yolk. Eggs laid by hens contained 11–19 µg of Se, with higher levels in the yolk. Higher Se intake in feed increased Se levels in eggs, favoring egg white distribution. This led to the utilization of eggs as a source of Se, particularly in selenium-enriched organic eggs, representing a modern “functional organic food” containing biologically available Se.

Antioxidant stability of chicken meat and Selenium

Numerous studies have documented the antioxidant effect of selenium (Se) on broiler chicken meat stability (Dlouhaet al., 2008; Skrivan et al., 2008; Wang et al., 2011c; Liao et al., 2012; Yang et al., 2012; Rama Rao et al., 2013). Including Se-Chlorella in broiler diets enhanced meat oxidative stability, as evidenced by reduced malondialdehyde values in breast meat after refrigeration (Dlouhaet al., 2008). Wang et al. (2011b) found that l-Se-Met and d-Se-Met supplementation increased Se concentration in serum and tissues, improving antioxidant capability and reducing drip loss of breast muscle compared to sodium selenite. Organic Se was shown to enhance body oxidation resistance more effectively than inorganic Se (Yang et al., 2012). Maternal Se-Met intake improved antioxidant status in 1-day-old chicks compared to sodium selenite, as indicated by increased enzyme activities and decreased malondialdehyde concentration (Wang et al., 2011a). Skrivan et al. (2012) observed that vitamin C reduced meat lipid oxidation, while selenized yeast effectively enriched meat with Se and increased antioxidant enzyme activities. Ahmad et al. (2012) found that selenium yeast and selenium yeast combined with sodium selenite increased antioxidant enzyme activities and oxidative stability of chicken breast meat more effectively than sodium selenite alone.

Selenium’s Influence on Glutathione Peroxidase Activity

Glutathione peroxidase (GSH-Px) is an enzyme crucial for converting harmful hydrogen peroxide into water and oxygen, with selenium (selenocysteine) playing a key role in its activation, likely by modifying the enzyme into GPx4. GSH-Px works synergistically with vitamin E to eliminate excessive peroxides, particularly those from lipid oxidation. Studies show that selenium concentration in broiler chicken diets positively correlates with plasma GSH-Px activity. Different selenium sources and levels significantly influence GSH-Px activity in meat, with selenium-enriched algae and yeast showing promising results. Organic selenium enhances body oxidation resistance more effectively than inorganic forms, as evidenced by higher serum GSH-Px activity in experimental groups. Since the enzyme itself cannot be directly supplied through food due to digestion, its concentration in the body is increased by providing its coenzyme, glutathione tripeptide.

Selenium’s Role in Immune Function

Selenium is crucial for both human and animal immune systems. Its deficiency can impair cellular and humoral immunity, while adequate intake strengthens immune function. Selenium stimulates the proliferation of activated T lymphocytes, enhances their maturation into cytotoxic lymphocytes, and boosts natural killer cell activity. This enhancement is linked to increased receptor numbers for interleukin-2, critical for clonal expansion and differentiation into cytotoxic T cells. Additionally, selenium insufficiency reduces levels of IgG and IgM antibodies, impacting humoral immunity.

Rama Rao et al. (2013) investigated the impact of supplemented organic selenium on immune response in broiler chickens, finding a linear increase in cell-mediated immunity with higher dietary selenium concentrations.

Conversely, Funari et al. (2012) observed no significant effect of selenium source or level on humoral immunity against Newcastle disease vaccine or sheep red blood cells. Additionally, Liao et al. (2012) found that selenium yeast increased tissue selenium retention, while Se protein (AMMS Se) was more effective in enhancing immune functions of heat-stressed broilers compared to inorganic selenium (Na2SeO3) or selenium yeast.

A low-selenium diet led to reduced activities of total antioxidant capacity, superoxide dismutase, and glutathione peroxidase, alongside increased xanthine oxidase activity and malondialdehyde content. This deficiency also resulted in lesions in immune organs, decreased serum interleukin-1β and interleukin-2 levels, and increased serum tumor necrosis factor content. These findings suggest that oxidative stress inhibited the development of immune organs and impaired the immune function of chickens (Zhang et al., 2012).

Selenium and Fatty Acids in Muscular Tissue

Pappas et al. (2012) investigated the impact of selenium on fatty acid composition and lipid stability in chicken breast muscle. They utilized a yeast source for selenium supplementation, resulting in selenium-enriched meat. Increasing selenium levels in the diets led to higher levels of health-promoting long-chain polyunsaturated fatty acids, while also reducing lipid oxidation at slaughter. This suggests that supplementing chicken diets with selenium, at levels below toxicity, enhances meat quality and preserves health-promoting fatty acids.

Zdunczyk et al. (2011) examined the effects of selenium and vitamin E on fatty acid profiles in broiler chicken breast muscles. They found that the muscle fat contained relatively high levels of omega-3 polyunsaturated fatty acids (PUFA), sourced from fish meal. However, no significant differences were observed in the fatty acid profiles of the muscle fat concerning selenium and vitamin E levels. Conversely, Kralik et al. (2012, 2013) noted increased proportions of omega-3 PUFA and decreased levels of monounsaturated fatty acids in muscle tissue following supplementation with organic selenium.

Selenium Intoxication

Inorganic selenium compounds are more toxic than organic ones. In terms of decreasing toxicity, the compounds can be ranked as follows: selenite > selenate > selenocysteine > methylated selenium compounds. Selenium acid is identified as the most toxic form of selenium (Barceloux, 1999). Bartik and Piskac (1974) classified selenium intoxication into three types: acute, sub-acute, and chronic poisoning (alkali disease). Acute intoxication is characterized by respiratory disorders, ataxia, diarrhea, or death, often accompanied by the distinctive garlic odor of breath due to the presence of methyl selenide. Chronic intoxication, resulting from prolonged exposure to high selenium levels in the diet, manifests as reduced feed intake, slowed growth, hair loss, liver cirrhosis, or anemia. Chronic poisoning, known as selenosis, predominantly occurs in regions with elevated selenium levels in soil and drinking water.

The range of selenium intake that is sufficient yet non-toxic for the organism is narrow and depends on the chemical form of selenium. Trials in rats demonstrated that selenium intake at 5 mg/kg of body weight led to growth retardation, while 6.4 mg/kg caused liver changes, and 8 mg/kg resulted in anemia and increased mortality. The mechanism behind growth retardation is reduced secretion of the growth hormone (WHO, 1996). For poultry, it’s recommended to include a selenium supplement of 0.5 mg/kg in complex feed mixes. Higher selenium levels in the diet can have adverse effects on animal health.


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