Aflatoxicosis alters avian renal function, calcium, and vitamin D metabolism.
Experiments were designed to determine the effects of aflatoxicosis on avian renal function, calcium (CA), inorganic phosphorous (Pi), and vitamin D metabolism, and to determine if the effects of aflatoxin are reversible upon discontinuation of toxin administration. Three-week-old male broiler chickens (n = 12 per treatment) received aflatoxin (AF; 2 mg/kg po) or an equal volume of corn oil, the AF carrier vehicle, for 10 consecutive days. After 10 d of treatment, half of the birds from each treatment group were anesthetized and prepared for renal function analysis, which included a 2-h phosphate loading period. Ten days after discontinuation of AF treatment, the remaining birds in each treatment group were anesthetized and prepared for renal function analysis. AF decreased plasma 25-hydroxy vitamin D [25(OH)D] and 1,25-dihydroxy vitamin D [1,25(OH)2D] levels after 5 d of treatment. After 10 d of treatment, urine flow rate (V), fractional sodium excretion (FENa), and fractional potassium excretion (FEK) were lower in AF-treated birds. In addition, total plasma Ca tended to be lower (p = .10) and fractional Ca excretion (FECa) tended to be higher (p = .10) in the AF-treated birds. Intravenous phosphate loading produced a sharp increase in urine hydrogen ion concentration ([H+]) in the AF-treated birds. Glomerular filtration rate (GFR) was reduced and plasma osmolality was increased in AF-treated birds 10 d after discontinuation of toxin administration. The results indicate that AF directly or indirectly affects Ca and Pi metabolism in avians. At the present time, the effects may be related to altered vitamin D and parathyroid hormone (PTH) metabolism. Aflatoxicosis may decrease endogenous PTH synthesis and the renal sensitivity to PTH. The AF-related increase in urine [H+] during phosphate loading is probably due to increased Na+/H+ counterport, suggesting that AF stimulates sodium reabsorption. Also, the decrease in GFR exhibited 10 d after toxin removal indicates that AF may cause prolonged alteration in renal function.
Glahn
R P
RP
Department of Animal and Poultry Sciences, University of Arkansas, Fayetteville 72701.
Beers
K W
KW
Bottje
W G
WG
Wideman
R F
RF
Huff
W E
WE
Thomas
W
W
D000348:Aflatoxins / Q000633:toxicity*; D000818:Animals; D001798:Blood Proteins / Q000032:analysis / Q000187:drug effects; D001835:Body Weight / Q000187:drug effects; D002118:Calcium / Q000097:blood / Q000378:metabolism*; D002645:Chickens; D007668:Kidney / Q000187:drug effects* / Q000502:physiology; D008297:Male; D015651:Mycotoxicosis / Q000378:metabolism / Q000503:physiopathology*; D009929:Organ Size / Q000187:drug effects; D010758:Phosphorus / Q000378:metabolism; D014807:Vitamin D / Q000097:blood / Q000378:metabolism*
D000348:Aflatoxins; D001798:Blood Proteins; D014807:Vitamin D; D010758:Phosphorus; D002118:Calcium