Selenium Contamination in Water. Группа авторов
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tissues, and nephritis (Faye and Seboussi 2008). Table 4.2 provides the recommended normal intake of selenium in animals per day.
4.3.1 Cattle
Toxicity in any animal depends on the different parameters or factors, such as forage organisms, animal feeding, and dietary components etc. Alkali disease or chronic cow toxicity occurs when 5–40 mg Se/kg BW diets are fed for several months. There is acute toxicity when eating feed, which contains 10–20 mg Se/kg BW (National Research Council [NRC] 1983). One research found that the feed conversion efficiency in young calves was affected by 10 mg Se/kg DM. The winter season is the most vulnerable to Se toxicity in dairy cattle, though handling Se‐enriched stall feed (Jenkins and Hidiroglou 1986; Ropstad et al. 1988). Se toxicity in animals has caused many symptoms, such as hair loss, coat roughness, dullness and lack of strength, emaciation, joint bone deterioration, higher respiration levels, weakness and lameness, hooves detachments, etc. (Ghosh et al. 1993; Rosenfeld and Beath 2013).
4.3.2 Sheep
Oral selenite exposure with 50 mg Se/day in sheep caused death after exposure for 72 days. Postmortem reports determined that lesions were observed in heart and lungs (Glenn et al. 1964a, 1964b). The seleniferous range caused severe eye deformation in growing lambs (Rosenfeld and Beath 1947). The erythrocytic lysis process was also reported after selenite exposure to sheep and this might explain the hematological changes in sheep due to chronic selenosis (Young et al. 1981).
Table 4.2 RDI of selenium ingestion for different animals.
Source: Adapted from Hosnedlova et al. (2017).
| Animal species | RDI of Se | References |
|---|---|---|
| Beef cattle | 100 μg/kg of FDM | National Research Council (NRC) (2001), Suttle (2010) |
| 0.20 mg/kg | McDowell (1992) | |
| Camel | 97–112 ng/ml | Zong‐Ping et al. (1994) |
| 25–53 ng/ml | Rahim (2005) | |
| Dairy cattle | 300 μg/kg of FDM | National Research Council (NRC) (2001), Suttle (2010) |
| 0.30 mg/kg | McDowell (1992) | |
| Donkeys | 2 mg/day | Geor et al. (2013) |
| 0.1–0.15 mg/100 kg BW | National Research Council (NRC) (2007) | |
| Goat | 0.1 mg/kg of FDM | Papazafeiriou et al. (2016) |
| Horses | 0.1 ppm of FDM | National Research Council (NRC) (2007), Pagan et al. (1999) |
| 0.10 mg/kg | McDowell (1992) | |
| Pigs | 0.15–0.30 mg/kg | Surai and Fisinin (2015) |
| Swine | 0.10–0.30 mg/kg | McDowell (1992) |
| Sheep | 0.1–0.2 mg/kg of FDM | National Research Council (NRC) (1985) |
| 0.10–0.20 mg/kg | McDowell (1992) |
BW – body weight; FDM – food dry matter; RDI – recommended daily intake.
Most of the studies indicated that toxicity in sheep and lambs was caused by 0.45–8 mg Se/kg LW (Caravaggi et al. 1970; Yaeger et al. 1998; Tiwary et al. 2006). Inorganic forms of Se caused toxicity in sheep and lambs. Giese (1984) found that most of the Se excreted via urine and feces after intravenous injection of high Se dose. The half‐life of Se in sheep is 14.7 days (Blodgett and Bevill 1987). Se toxicity in sheep and lamb caused respiratory problems, hair loss, cracks on hooves and horn, ataxia, and reduced feed intake. Myocardial necrosis and pulmonary alveolar vasculitis were found after exposing lambs with 8 mg Se/kg LW (Gupta et al. 1982; Tiwary et al. 2006).
4.3.3 Pigs
Miller and Williams (1940) reported that oral selenite intoxication with swine body weight of 13–23 mg Se/kg caused paresis, tremor, vomiting, anorexia, diarrhea, and depression (Figure 4.1). 10 ppm of sowing exposure results in toxicity, shown by reduced design rate, litter size, and piglet weight (Wahlstrom and Olson 1959). A study by Diehl et al. (1975) reported that 2.0 and 1.2 mg/kg body weight administration caused muscle tetany, increased plasma glutamic oxaloacetic transaminase (GOT) activity, and clinical signs of tremor, ataxia, etc. As observed in sheep and calves, acute and chronic Se toxicity has also emerged in young pigs. Acute Se toxicity in young lambs following selenosis manifested similar symptoms (Shortridge et al. 1971). Chronic Se toxicity induced sluggishness, lack of energy, emaciation, hair roughness, hair loss, sluggishness of hooves, damage to the liver, heart failure, etc. (Underwood 1979).
Figure 4.1 (a and b) Symptoms of selenosis in pigs (unthriftiness (a) and separation of the hoofs from the skin (b)).
(Source: Adapted from Wahlstrom et al. (1956)).
Toxicity varies according to the pigs’ genetic difference. Some of the studies have reported that pigs’ susceptibility to Se toxicity varied depending on pigs’ hair color (Wahlstrom and Olson 1959; Wahlstrom et al. 1984). Red‐haired pigs were more prone to Se toxicity than black‐ or white‐haired pigs (Wahlstrom et al. 1984). 4–8 mg Se/kg DM exerts Se toxicity in pigs in food grains; that also depends on the composition of food and other factors such as duration of exposure (Palmer et al. 1983; Goehring et al. 1984a; Goehring et al. 1984b). One study of a maize‐soybean diet with 8 mg Se/kg DM impaired appetite and growth within five weeks of exposure. However, for the same time duration this concentration in wheat and oats had no effect on the pigs (Goehring et al. 1984a; Goehring et al. 1984b). 12 mg Se/kg DM of feed caused hoof lesions in pigs, as in dairy cattle and horses (Goehring et al. 1984b). The concentration in pigs with 5, 10, and 25 mg Se/kg DM for 120 days resulted in hoof lesion, edema, hyperemia, extreme spinal cord lesions, paralysis of the body, emaciation, postnecrotic atrophic liver cirrhosis, and lumbal poliomyelomalacia, etc. and inflammation (Goehring et al. 1984b; O'Toole and Raisbeck 1995). Feeding meal diets of corn‐soybean along with 5 ppm of Se in swine results reduced growth and feed intake. The most influential measure of toxicity to Se is decreased growth rate. Up to 8.3 ppm Se addition in swine feed did not cause any health effects but after 12 ppm Se meal exposure caused hoof lesions (Mahan and Moxon 1980; Wahlstrom et al. 1984; Goehring et al. 1984b). The same diagnosis of hoof lesions was also published for Harrison et al. (1983) after exposure to Se. Poulsen et al. (1989) reported that after suckling the growth