selenium Flashcards
What are the forms of selenium?
- Soil characteristics are important:
-
Selenate (SeO4-2)
- Easily absorbed by plants
- Associated with well aerated alkaline soils
-
Selenite (SeO3-2)
- Predominate in acidic soils
- Poorly absorbed by plants
- Selenide (Se-2)
- Uncommon
- typically found as metal-Se crystals
- Elemental Selenium
- Rare
-
Selenate (SeO4-2)
What enzymes is selenium are part of ?
- Glutathione peroxidase
- Thioredoxin reductase
- others
What does selenium deficiency cause?
nutritional muscular dystrophy
What is important about selenium’s safety margin?
- Narrow safety margin
- Small difference between deficiency and toxicity
What functions does selenium perform in the body?
- Cellular antioxidant
- Glutathione reductase, Thyroxin formation
- Competes with S, replaces sulfur in AA
What are obligate Se Accumulators? What are some examples of these plants?
- REquire Se for growth
- Accumulate very high Se levels (up to 10,000 ppm)
- Unpalatable
- Useful as indicators of seleniferous soil
- Genera include Astragalu, Oonopsis, Stanleya and Xylorrhiza
What are facultative Se Accumulators? What are some examples of these plants?
- Do NOT require Se for growth, but accumulate high Se levels (up to 100 ppm)
- Unpalatable
- Genera include: Atriplex, Machaeranthera and Sideranthus
What plants are responsible for the majority of selenium poisonings and why?
- Grains and Grasses
- Accumulate 1-25 ppm
- remain palatable
What are sources for selenium poisoning?
- Feed supplements
- up to 0.3 ppm Se added to feed
- Accidental mis-mixes occur
- feeding chelated forms instead of organic
- Injectable Se products
- using 2 Se containing products imulaneously
- Doubling the dose
- Poor weight estimates
How is Selenium absorbed and eliminated in the body?
- Absorbed relatively efficiently (35- 85% depending on form)
- Plant Se more bioavailable
- Elimination primarily via urine and feces
How is Selenium absorbed and eliminated in the body?
- Absorbed relatively efficiently (35- 85% depending on form)
- Plant Se more bioavailable
- Elimination primarily via urine and feces
What is the MOA of Se?
- Poorly defined - likely a combo
- Production of free radicals ⇢ oxidative tissue damage
- Displacement of S from proteins
- Selenocysteine and selenomethionine are similar to cysteine and methionine
- Likely mechanism in hair and hoof lesions of chronic toxicosis
- Depress ATP synthesis; vascular damage
What are the 3 clinical syndromes of Se Toxicosis?
- Acute
- Subacute
- Chronic
What does Acute Selenium toxicosis look like?
- Usually Iatrogenic
- Plants with high Se are unpalatable
- Progressively worsening weakness, ataxia, and dyspnea in 1-24 hrs
- Vomiting (swine)
- Death in <48hr
-
Occasionally no obvious signs, but sudden death with signs of heart failure:
- Pulmonary edema
- Generalized congestion
- Petechia and ecchymosis in epicardium and endocardium
- Hydrothorax and hydropericardium
What is the treatment for Acute Selenosis?
- None effective - animals often die quickly after injection
- General treatment for shock
- Antioxidants:
- acetylcysteine (140 mg/ml)
- Sodium thiosulfate (300-600 mg/kg IV) LA
What is Subacute (subchronic?) selenosis?
- In pegs fed high Se diets (10-27 ppm)
- 2-6 weeks
- 0.3 ppm is legal limit
- Hindlimb ataxia ⇢ progressive
- posterior paralysis and tetraparalysis
- Hoof separation
- Animals remain alert
How is Subchronic Selenosis diagnosed?
- Histopath: Bilateral poliomalacia of spinal cord
- Measure Se in Feed (>4 ppm)
- Measure Se in Liver (>3 ppm)
What is Chronic Selenosis?
- “Alkali Disease”
- Usually after >30 days exposure to seleniferous grains and forages
- Weight loss; bilateral, symmetrical alopecia, rough hair coat
- Especially nape of neck and tail
- Lameness
- Swelling and erythema of coronary bands
- Hoof separation and/or abnormal hoof growth
- degenerative joint disease
- Immunosuppression
- blocks primary antibody response
- Decreased fertility
- Anemia
- Weight loss; bilateral, symmetrical alopecia, rough hair coat
How is Selenium toxicosis diagnosed?
- Se in whole blood, serum, liver, feed, or forage
- Whole blood is easiest and most practical
- Better than serum
- Se in hair
- Se in hoof wall
What is the treatment for selenium toxicosis?
- No good treatment - focus on prevention
- terminate exposure
- Primarily supportive - NSAIDS
- Low Se and High S diet
What are the differential for Acute Selenium toxicosis?
- Se deficiency
- Gossypol
- Organophosphates/carbamates
- Enterotoxaemia
What are the differential for Chronic selenium toxicity?
- Laminitis from grain overload
- Ergotism
- Fescue foot
- Fluorosis
- Frostbite of the feet
What are the differentials for subchronic selenium toxicosis in pigs
- Metabolic bone disease
- Vit B deficiencies
- Cu deficiency
- Organic arsenic
What is the result of Vitamin E/Selenium Deficiency?
- White muscle disease
- Nutritional Muscular Dystrophy
- Mulberry heart disease (hepatosis dietectica)
