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Biomedical subjects

J R Manaligod

Publications and source records attributed to J R Manaligod.

42 records · Page 3Linked to original sources

Biochemical, morphological and hybrid studies in hyperprolinemic mice.

Hyperprolinemia, hyperprolinuria and hydroxyprolinuria were observed in PRO/Re mice. Hepatic proline oxidase activity in PRO/Re mice was markedly deficient. It was demonstrated that the deficiency of proline oxidase activity was not due to the presence of an inhibitor. The mutant enzyme in PRO/Re showed no difference in heat stability but had a poor affinity for the substrate, L-proline as compared to normal enzymes. There was no significant proteinuria or hematuria in PRO/Re mice. Their serum protein and blood urea nitrogen were normal. Morphologic studies by light and electron microscopy demonstrated no abnormality in the renal tissues of PRO/Re up to 6 months of age, suggesting that hyperprolinemia did not cause renal damage. Pedigree studies showed that F1 generation (PRO/Re x CD 1) had approximately 50 percent of normal proline oxidase activity and significantly higher plasma proline. The distribution of hepatic proline oxidase activity in F2 GENERATION (F1 x F1) was characteristic of an autosomal recessive trait.

Amino Acid Metabolism, Inborn Errors↗

Effects of prenatal ethanol exposure on postnatal renal function and structure in the rat.

Effects of prenatal ethanol exposure on postnatal renal function and structure in the rat. Renal function and morphology were studied in 90-day-old offspring of ethanol-fed (E) rats and were compared to pair-fed control (C) animals. Compared to C rats, E rats were smaller at birth, had higher fractional sodium excretion (p less than 0.01) and lower fractional potassium excretion (p less than 0.01). In E rats, sodium (Na) restriction resulted in a significant increase in urine flow and Na wastage, whereas C rats remained in Na balance. E rats developed hyperkalemia, when potassium (K) intake was increased from 2.8 to 14 mEq/day. Baseline creatinine clearance, urine and blood osmolalities and pH, plasma electrolytes and aldosterone concentrations were similar in both groups. There was no significant difference in wet or dry kidney weight, renal water content, or renal tissue concentrations of Na or K between the two groups. No difference was found in gross morphology or light microscopic appearances of the kidneys between E and C rats. Thus rats exposed to ethanol during fetal life have a defect in urine concentration and Na conservation when fed a low Na diet and a defect in K excretion when given a K load without evidence of any gross or light microscopic renal structural abnormalities at 90 days of age.

Animals↗