1938; Landauer 1940; Cantor et al. 1984). Table 4.3 lists more research on the toxicity caused by Se.
Figure 4.2 (a) The liver section of poultry birds that had ingested selenium showing congestion in blood vessels, congestion in sinusoids, necrosis in the parenchyma, and connective tissue proliferation between the lobules
(Source: Adapted from Kumar et al. (2018)).
(b) Section of birds’ lungs showing congestion in the alveoli and oedema in the bronchi
(Source: Adapted from Kumar et al. (2018)).
(c) Kidney section of poultry birds that had ingested selenium showing degeneration of tubules, infiltrations of mononuclear cells
(Source: Adapted from Kumar et al. (2018)).
(d) Section of cerebellum of birds that had ingested selenium showing degeneration of Purkinje cells
(Source: Adapted from Kumar et al. (2018)).
Table 4.3 Se toxicity in poultry birds.
| Chemical form | Age | Dose (ppm) | Toxic effects | References |
|---|---|---|---|---|
| Na2SeO3 + Se in wheat | Immature | 10 | Growth ↓ | Carlson and Leitis (1957) |
| Se in wheat | Laying hens | 10 | Hatchability ↓ | Moxon and Wilson (1944) |
| Se in corn, barley, wheat | Adult | 5 | Mortality ↑ | Moxon (1937) |
| Na2SeO3 | Adult | 6.5 | Deformed embryos | Moxon (1937) |
| Na2SeO3 | One day | 8 | Body weight ↓ | Moxon (1937) |
| Selenous acid | One day | 8 | Mortality ↑ | Thapar et al. (1969) |
| SeO2 | one day | 5 | Mortality ↑ | Hill (1979) |
| Na2SeO3 | Adult | 8 | Dead embryo | Gruenwald (1958) |
| Selenite | Adult | 10 | Growth ↓ | Jensen and Chang (1976) |
| Selenite | One day | 5 | Growth ↓ | Jensen (1986) |
↑ – Increased; ↓ – Decreased; Na2SeO3 – Sodium selenite, SeO2 – Selenium dioxide; ppm – parts per million.
4.3.5 Camel and Horse
To date, only experimental selenosis in camels has been reported. One study by McDonald et al. (2011) reported that Se doses with 1 and 2 mg/kg body weight caused lassitude, inappetence, inability to raise, mild pulmonary congestion, alveolar edema, acute myositis, and edema in a different portion of the brain. Administration of 0.051–0.095 mg Se/kg LW to camels caused selenosis (Seboussi et al. 2008). Faye and Seboussi et al. (2008) reported that 8 and 12 mg Se/day administration caused several clinical symptoms such as hair discoloration, followed by alopecia, dark watery diarrhea, inferior cervical lymph increase, dyspneic respiration, and difficulty in walking. Pathological alterations in kidney, heart, and liver were also observed, such as congestions in Bowman's space and convoluted tubules, the proliferation of Purkinje fibers, degenerative changes in myofibers, degenerative changes hepatic cells of the hepatic lobules, edema in intercostal and diaphragm muscles, perivascular edema in brain, etc. (Figure 4.3a–l). Aitken (2001) reported that selenosis showed mainly hoof lesions in horses, along with decreased body growth.
4.3.6 Antelope
Raisbeck et al. (1995) studied the impact of Se on antelope treatment. For a month, antelopes were given water with <50 ppb Se. Following the acclimation one group of antelopes was fed for 168 days with 25 ppm Se native grass hay along with alfalfa hay (0.3 ppm Se). The final exposed Se concentration was of 15 ppm. The control group was given feed with approximately 0.3 ppm Se. After the experiment it was found that the higher exposure to Se caused a reduction in antelopes’ feed intake and a reduction in body weight. However, there were no lung, liver, or kidney abnormalities.
Figure 4.3 (a) Alopecia; (b) pad lesions; (c) sternal position; (d) hypertrophy of cervial lymphnoid; (e) heart congestion, soft discoloration; (f) liver congestion; (g) pulmunary congestion; (h) brain edema; (i) muscle discoloration; (j) camel heart congestion in capillary vessels; (k) degeneracy of liver in camel; (l) toxic effects in kidney of camel
(Source: Adapted from Seboussi et al. (2012)).
4.4 Control Measures of Selenium Toxicity
All of the previous reports have mentioned that Se toxicity could reduce livestock farming industry production
