↑ – 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 in any country. Mapping of agricultural land based on the presence of compulsory and optional Se accumulator plants and non‐accumulator plants is the ultimate control measure method (de Souza et al. 1999; Barillas et al. 2011; White 2016; Gupta and Gupta 2017; Schiavon and Pilon‐Smits 2017). It will help to decide the measure of grazing land and actively manage the toxicity of Se in the soil. Before applying forage plants to animals of livestock or any other supplements these should be subjected to determination of the level of Se. Both of these preventive steps would potentially minimize the intake of Se in livestock (Tiwary et al. 2006). Transgenic plants have the potential to remove Se from soil (Pilon‐Smits and LeDuc 2009). Apart from these etiological preventive steps, some studies stated that the amount of animal blood Se can be a great predictor for earlier determination of signs linked to Se toxicity. The presence of >1.5 μg/ml in cattle blood has been reported to be indicative of the onset of Se toxicity (Deore et al. 2002).
Preventive measures such as soil treatment, high protein‐rich feed feeding, dietary sulfate, methionine supplement, linseed meal, spraying sulfur‐containing materials on fodders grown in selenium‐rich soil, clean water, etc. may reduce selenosis (Prakash et al. 2010; He et al. 2018; Wadgaonkar et al. 2018). To date, no particular studies have ever reported absolute attenuation of Se toxicity in animals as a result of the procedure. The study on intravenous administration of reduced glutathione (GSH) @ 5 mg/kg of BW was useful in arresting the Se toxicity after decreasing the activity of glutathione peroxidase (GSH‐Px) (Deore et al. 2005). The study of Arora et al. (1975) and Arora (1985) reported that trace mineral mixture which includes 1 kg of magnesium sulfate (MgSO4), 166 g of ferrous sulfate (FeSO4), 24 g of copper sulfate (CuSO4), 75 g of zinc sulfate (ZnSO4), and 15 g of cobalt sulfate (CoSO4) was a great help in recovering the Se toxicity in buffaloes after 21 days of exposure and within 50 days. One research recorded that both arsanilic acid (0.02%) and 3‐nitro (0.005%) were similarly successful in preventing selenosis in pigs. These chemicals also had positive effects on weight gain as the control pigs developed between 67 and 100 pounds per pig (Wahlstrom et al. 1956). Se toxicity was also minimized by a protein‐rich diet and mineral balance mixture in buffaloes (Fessler et al. 2003). Increasing horse grazing time to 50% on pasture significantly reduced Se concentration compared to those horses that had less pasture time (Crisman et al. 1994). The same pattern emerged in water buffaloes (Khanal and Knight 2010).
Seleniferous soil is the primary component in the food chain which transfers the higher levels of Se. Adding sulfur decreases the plant supply Se in soil. One piece of research suggested that the introduction of 1000 kg gypsum/ha in sugar cane increased the S:Se ratio and decreased the Se amount (Dhillon and Dhillon 1991). Continuous application of S can result in plant selenium deficiency, and eventually there will be trouble for domestic animals (Andrews et al. 1968; McDonald 1975; Fessler et al. 2003). One phytoremediation technique was reported to reduce the level of Se in soil, where it was claimed that kenaf and canola planting in seleniferous soil had scavenged the Se from soil and water (Wood 2000).
Carbohydrate‐rich diets, protein, sulfate, and calcium in cattle decreased Se levels (Kessler 1993). Concentration above 2.4 g/kg DM of sulfur decreased Se absorption substantially (Spears and Weiss 2008). Administration of 0.8% calcium DM in feed significantly decreases Se in pregnant cows' blood and muscle (Harrison et al. 1983).
Vitamin E administration can reduce the toxicity to Se in cattle (NRC 1996). One study suggested that the use of vitamin E in dairy cattle with 15–60 foreign units (IU) decreases Se (NRC 1984, 1996).