selenium

Question 1

What are the forms of selenium?

Answer 1

• 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

Question 2

What enzymes is selenium are part of ?

Answer 2

• Glutathione peroxidase
• Thioredoxin reductase
• others

Question 3

What does selenium deficiency cause?

Answer 3

nutritional muscular dystrophy

Question 4

What is important about selenium’s safety margin?

Answer 4

• Narrow safety margin
  
  • Small difference between deficiency and toxicity

Question 5

What functions does selenium perform in the body?

Answer 5

• Cellular antioxidant
• Glutathione reductase, Thyroxin formation
• Competes with S, replaces sulfur in AA

Question 6

What are obligate Se Accumulators? What are some examples of these plants?

Answer 6

• 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

Question 7

What are facultative Se Accumulators? What are some examples of these plants?

Answer 7

• Do NOT require Se for growth, but accumulate high Se levels (up to 100 ppm)
• Unpalatable
• Genera include: Atriplex, Machaeranthera and Sideranthus

Question 8

What plants are responsible for the majority of selenium poisonings and why?

Answer 8

• Grains and Grasses
• Accumulate 1-25 ppm
• remain palatable

Question 9

What are sources for selenium poisoning?

Answer 9

• 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

Question 10

How is Selenium absorbed and eliminated in the body?

Answer 10

• Absorbed relatively efficiently (35- 85% depending on form)
  
  • Plant Se more bioavailable
• Elimination primarily via urine and feces

Question 10

How is Selenium absorbed and eliminated in the body?

Answer 10

• Absorbed relatively efficiently (35- 85% depending on form)
  
  • Plant Se more bioavailable
• Elimination primarily via urine and feces

Question 11

What is the MOA of Se?

Answer 11

• 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

Question 12

What are the 3 clinical syndromes of Se Toxicosis?

Answer 12

• Acute
• Subacute
• Chronic

Question 13

What does Acute Selenium toxicosis look like?

Answer 13

• 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

Question 14

What is the treatment for Acute Selenosis?

Answer 14

• 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

Question 15

What is Subacute (subchronic?) selenosis?

Answer 15

• 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

Question 16

How is Subchronic Selenosis diagnosed?

Answer 16

• Histopath: Bilateral poliomalacia of spinal cord
• Measure Se in Feed (>4 ppm)
• Measure Se in Liver (>3 ppm)

Question 17

What is Chronic Selenosis?

Answer 17

• “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

Question 18

How is Selenium toxicosis diagnosed?

Answer 18

• 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

Question 19

What is the treatment for selenium toxicosis?

Answer 19

• No good treatment - focus on prevention
• terminate exposure
• Primarily supportive - NSAIDS
• Low Se and High S diet

Question 20

What are the differential for Acute Selenium toxicosis?

Answer 20

• Se deficiency
• Gossypol
• Organophosphates/carbamates
• Enterotoxaemia

Question 21

What are the differential for Chronic selenium toxicity?

Answer 21

• Laminitis from grain overload
• Ergotism
• Fescue foot
• Fluorosis
• Frostbite of the feet

Question 22

What are the differentials for subchronic selenium toxicosis in pigs

Answer 22

• Metabolic bone disease
• Vit B deficiencies
• Cu deficiency
• Organic arsenic

Question 23

What is the result of Vitamin E/Selenium Deficiency?

Answer 23

• White muscle disease
• Nutritional Muscular Dystrophy
• Mulberry heart disease (hepatosis dietectica)