Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020639 (hypoproteinemia)
 1,134 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Several studies indicate the pathophysiological importance of reactive oxygen species in rats with nephrotic syndrome induced by puromycin aminonucleoside, an experimental model of the human minimal change disease. The role of reactive oxygen species in these rats was further evaluated, examining the effect of dietary deficiency and supplementation of antioxidants (vitamin E and selenium) on biochemical and renal ultrastructural alterations induced by puromycin aminonucleoside. Male Wistar rats, weaned at 3 weeks, were placed on diets normal, deficient or supplemented in vitamin E and selenium for 4 weeks. At the end of this period, rats were divided in two groups: control (sacrificed without any further treatment) and nephrotic (injected with puromycin aminonucleoside and sacrificed 7 and 22 days later). In control rats, the dietary deficiency or supplementation of antioxidants resulted in no significative differences in renal function, proteinuria or kidney ultrastructure. However, kidney lipoperoxidation, kidney glutathione peroxidase activity and circulating levels of vitamin E changed according to the amount of antioxidants in the diet. Seven days after the injection of puromycin aminonucleoside, rats fed normal, deficient or supplemented diets, developed nephrotic syndrome. However, proteinuria, hypoproteinemia, renal dysfunction and ultrastructural alterations were higher in rats fed a deficient diet. In contrast, proteinuria and kidney ultrastructural alterations were lower in rats fed a supplemented diet. Kidney lipoperoxidation and glutathione peroxidase activity increased on day 7 in rats fed a normal or a deficient diet, but not in rats fed a supplemented diet. This study shows that nephrotic syndrome induced by puromycin aminonucleoside in rats is modified by dietary antioxidants (vitamin E and selenium). Dietary supplementation ameliorates it and dietary deficiency exacerbates it.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of dietary antioxidants on puromycin aminonucleoside nephrotic syndrome. 764 24

The possible role of Commiphora molmol emulsion (CME) in protecting against lead (PbAc)-induced hepatotoxicity, oxidative stress and immunotoxicity in rabbits was assessed. Six groups of animals were used: groups I (control) and II (PbAc) were not supplemented with CME. Groups III (CME50) and IV (CME50+PbAc) were administered with CME in a dose rate of 50mg/kg bwt, while groups V (CME100) and VI (CME100+PbAc) were received 100mg CME/kg bwt daily p.o for successive 14 weeks. Groups II, IV and VI were given 80 mg PbAc/kg bwt/day orally for 6 weeks starting from the 9th week. At the 12th week, animals were subjected to immunization by a single dose of sheep RBCs. The PbAc-group showed 220% increase in hepatic malondialdehyde levels, while glutathione, glutathione s-transferase and glutathione peroxidase levels decreased. Lead-acetate induced hypoproteinemia and hypoalbuminemia, and increased aminotransferases activity. It reduced the values of lymphocyte transformation test, phagocytic activity, phagocytic index and antibody titer against sheep SRBCs. Interestingly, pretreatment with CME attenuated these adverse effects in a dose-dependent protection. CME, therefore, is a potent antioxidant, and can protect against PbAc-induced hepatic oxidative damage and immunotoxicity by reducing lipid peroxidation and enhancing the antioxidant and immune defense mechanisms.
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PMID:Oxidative stress and immunotoxic effects of lead and their amelioration with myrrh (Commiphora molmol) emulsion. 1981 24