| First Author | Kanwar YS | Year | 1975 |
| Journal | Biomedicine | Volume | 22 |
| Issue | 3 | Pages | 209-16 |
| PubMed ID | 240452 | Mgi Jnum | J:25846 |
| Mgi Id | MGI:73561 | Citation | Kanwar YS, et al. (1975) Biochemical, morphological and hybrid studies in hyperprolinemic mice. Biomedicines 22(3):209-16 |
| abstractText | 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. |
