|Nielsen, Forrest - Frosty|
Submitted to: Journal of Federation of American Societies for Experimental Biology
Publication Type: Abstract only
Publication Acceptance Date: 12/10/1999
Publication Date: 3/15/2000
Citation: Yokoi, K., Uthus, E.O., Nielsen, F.H. 2000. Dietary homocystine induces renal damage in rats [abstract]. The Federation of American Societies for Experimental Biology Journal. 14:A796. Interpretive Summary:
Technical Abstract: Homocysteine is an endogenous atherogenic substance. A clinical case of homocystinuria associated with hematuria and proteinuria is known. Thus, an experiment was performed to examine the effect of dietary homocystine on selected biochemical parameters related to kidney function in rats. Ninety-five weanling male Sprague-Dawley rats were separated into 12 groups and fed respectively 3 x 2 x 2 factorially arranged diets: no supplemental sulfur amino acid (NSAA), 10 g/kg dl-methionine (MET) or 10 g/kg dl-homocystine (HCY); 0 or 7 mg/kg supplemental pyridoxine; 0 or 1 mg/kg supplemental nickel. The basal diet contained about 4.7 g of MET, 1.8 mg of vitamin B6 and 8 ng of nickel per kg. Twenty hour-urine was collected with fasting after 9 weeks feeding. Blood and tissue specimens were collected under ethyl ether anesthesia after 10 weeks. Dietary sulfur amino acid did not affect final body weight. HCY increased urinary protein loss, urinary albumin loss, urinary inorganic phosphate excretion, urinary allantoin excretion, relative kidney weight, aorta weight, plasma ammonia, and plasma homocysteine. Plasma albumin was lower in HCY than NSAA or MET- fed rats. Hemoglobinuria was observed in 18 of 31 rats fed HCY, compared to 0 of 32 rats fed NSAA and 1 of 32 rats fed MET. HCY increased plasma cholesterol and plasma phospholipids. HCY and MET increased urinary ammonia excretion and urinary sulfate excretion. The findings suggest that dietary homocystine can affect normal kidney function.