selenium toxicity final pptx

Selenium is one of important metal.

1. SELENIUM TOXICITY Presented by: Manisha Ghimire B.V.Sc And AH 7 th semester

2. Introduction Selenium (Se) is an essential trace element for animals and humans Its potency as a nutrient and a toxicant is such that few people have seen the pure element. narrow margin between too little and too much Daily requirement of selenium in diet  100 μg /kg DM for the beef cattle 300 μg /kg DM for dairy cows Toxic dose 8-10mg/kg

3. Selenium (Se) is a metalloid that exists as various forms red amorphous powder reddish crystal or brown-black solid. Selenium has four natural oxidation states: Selenide (+2) Elemental (0) Selenite (+4) and Selenate (+6) Organic forms selenomethionine and selenocysteine Inorganic form

4. Available in Nepal

5. EPIDEMIOLOGY Marco Polo, in 1295, described chronic selenium poisoining in horses ingesting certain plants . Signs were :lose mane , tail hair and slough hooves The first account of selenium poisoning in the U.S. was given by Dr. T.C. Madison in 1856 . (horses ,Missouri river) Poisoning is most common in grazing animals such as cattle, sheep, and horses, which may forage on seleniferous grasses, forbs or shrubs. Poultry , swine are susceptible if given seleniferous grains or diet.

6. Sources Obligate indicator plants require (100 – 10000 ppm) for growth and survival. accumulate selenium as water-soluble amino acid analogs of cysteine and methionine. Eg Astralagus (locoweed) and Oonopsis ( goldenweed ). Facultative indicator plants (25 – 100 ppm) . Eg Sideranthus and Atriplex ( saltbrush ). Non-accumulator plants may accumulate selenium upto 1-25ppm. Feed supplements, injectable drugs, industrial and commercial sources and seafood are the other sources of selenium. Industrial and commercial sources include photoelectric cells, glass and ceramics Fish and shellfish (not toxic level)

7. Selenium containing plants Plants preferentially accumulate inorganic forms and transform into organic forms . Inorganic forms of selenium is highly absorbed by plants because this form readily dissolve in water and is less bound to soil particles . Barley , wheat , and alfalfa accumulate more than 5ppm selenium

8. locoweed saltbush Goldenweed

9. 2

10. Mechanism of Action of Selenium toxicity Selenium replaces Sulphur in amino acids such as Cysteine and Methionine which results in synthesis of abnormal structural and enzymatic proteins. Depletion of intermediate substrate such as Glutathione and S- adenosyl methionine which disturbs their respective enzyme activities. Production of free radicals by reaction of selenium with thiols causing oxidative tissue damage. The cytotoxic activity of Selenium results from pro-oxidant catalytic activity of Selenide anions which produce Superoxide ions, H2O2 and other metabolic radicals.

11. Chronic Selenosis depresses ATP formation by reduction of sulphydryl -containing enzymes such as Succinic acid dehydrogenase and other dehydrogenases. Tissue Ascorbic acid decreases due to increased oxidation by ascorbic oxidases. This contributes to vascular damage caused by selenosis . GI lesions occur mainly due to irritant nature of Selenium.

12. Toxicity Maximum tolerable dose for cattle, sheep and horse range from 1 to 5 ppm while its daily requirement is 0.1 to 0.3 ppm in diet. It may cause acute, subacute or chronic poisoning. Selenious acid is the most toxic form of Selenium. Acute poisoning: 1 to 5 mg/kg orally and 0.5 mg/kg parenterally Subacute poisoning : 3 ppm for 3 days or more Chronic poisoning: 5-10 ppm Se for several weeks in cattle, swine, horse

13. Clinical Signs Acute toxicity ( Blind Staggers ) Lethargy, unresponsiveness, colic, bloat, dark watery diarrhoea , quickened and weak heartbeats, dyspnoea , frothing from nostrils, polyuria, cyanosis, weakness, uncertain gait, prostration, coma and death in 1-2 days in ruminants. Poliomyelomalacia in swine

14. Subacute toxicity Lowered conception rate and increase in a number of piglets born dead. Birds show low hatchability and embryos are usually deformed without beaks and with ropy feathers.

15. Chronic toxicity (Alkali Disease) Pronounced anemia A garlic odour from breathe occur.

16. Clinical Pathology Non significant alterations were recorded in mean values of Hb, PCV, TLC and TEC

17. Postmortem Findings Acute toxicoses causes congestion of organs, gastroenteritis, renal necrosis and hemorrhages, hydrothorax, pulmonary edema, pale cardiac muscles, etc. In subacute form, congestion and necrosis of liver and renal medulla, epicardial petechiae , abomasal and intestinal ulceration, erosion of articular surfaces (particularly tibia) occur. Transverse lines of abnormal growth occurs in hooves, cardiomyopathy and chronic fibroses or cirrhosis occurs.

18. Diagnosis History of feeding in selenium rich soil Sign and symptoms definitive diagnosis is based on assessments of selenium concentrations in serum, blood, tissue, feed, forage, and supplements. Glutathione peroxidase activity can be used to diagnose selenium deficiency, but is less useful in the diagnosis of selenium toxicosis. The liver and kidneys are the most common postmortem samples used for selenium analysis. Kidney selenium concentrations are higher than liver concentrations; however, in cases of toxicosis, this ratio can be reversed The liver selenium concentration increases rapidly after parenteral selenium supplementation.

19. Treatment Saline purgatives such as magnesium sulphate to eliminate selenium from gut. Acute Selenosis Oxygen therapy and treatment of pulmonary edema. Acetylcysteine as substitute of depleted glutathione at the loading dose of 140mg /kg body weight by I.V route followed by 70 mg/kg daily in 4 divided doses. Subacute and chronic selenosis Addition of substances in the diet that antagonise or inhibit toxic effects of Se. Examples: linseed oil meal, arsenic, silver, copper, and cadmium. Treatment of soil to reduce Se uptake

20. Contraindications Dimercaprol : inhibits the recovery from Se poisoning. Vitamin E : synergistic action with Se.

21. Prevention and Control Intensive sampling of herbage for Se analysis can be used to identify the most dangerous parts of the farm. Graze the less dangerous fields. Application of sulfur-containing materials e.g. sulfate of ammonia or gypsum, can reduce the levels of Se in herbage. If signs of toxicity arise on winter feed, additional safe feed should be used to dilute the toxic feed and the oral sulfate-dosing regime can be tried. Se should be removed from all mineral supplements of concentrate rations used on Se toxic farms. If other measures can not be used, cattle should be grazed in preference to horses in potentially toxic areas

22. References 1)Anup Giri , P. R. ,Vijay K. B. (2021). Selenium Toxicity in Domestic Animals. 2)Clark, R. F. (1996). Selenium Poisoning From a Nutritional Supplement. JAMA: The Journal of the American Medical Association, 275(14), 1087. https://doi.org/10.1001/jama.1996.03530380029025 3)Desta, B., Maldonado, G., Reid, H., Puschner , B., Maxwell, J., Agasan , A., Humphreys, L., & Holt, T. (2011). Acute selenium toxicosis in polo ponies. Journal of Veterinary Diagnostic Investigation, 23(3), 623–628. https://doi.org/10.1177/1040638711404142 4)D.K. Grewal, S. N. S. R. and C. S. R. (2016). Grewal, D.K., et al. "Chronic selenosis in dairy animal--a study of clinical observations and haematological profile. 17. 5)K. J. JENKINS and M. HIDIROGLOU. (1972). A REVIEW OF SELENIUM/VITAMIN E RESPONSIVE PROBLEMS IN LIVESTOCK: A CASE FOR SELENIUM AS A FEED ADDITIVE IN CANADA. 52. 6)Lynn F. James and James L. Shupe. (1984). Selenium poisoining in Livestock. 7) Mézes , M. and B. K. (2009). (n.d.). Prooxidant mechanisms of selenium toxicity –. 8)PAM Rogers(1), S. A. G. F. R. C. & J. M. (n.d.). Selenium toxicity in farm animals: treatment and prevention. 9)“Preventing Selenium Poisoning in Growing and Fattening Pigs” by R. C. Wahlstrom, L. D. Kamstra et al. (n.d.). Retrieved May 19, 2023, from https://openprairie.sdstate.edu/agexperimentsta_bulletins/456/?utm_source=openprairie.sdstate .edu%2Fagexperimentsta_bulletins%2F456&utm_medium= PDF&utm_campaign = PDFCoverPages 10) Raisbeck , M. F. (2020). Selenosis in Ruminants. Veterinary Clinics of North America: Food Animal Practice, 36(3), 775–789. https://doi.org/10.1016/J.CVFA.2020.08.013 11)Selenium Toxicosis in Animals - Toxicology - MSD Veterinary Manual. (n.d.). Retrieved May 19, 2023,

23. Thank You!!