Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019209 (hepatomegaly)
5,798 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The consequences of chronic corticosterone-induced stress (CCIS) on ascorbic acid (AsA) metabolism in chickens, an animal that syntheses the vitamin, are not known. This study was conducted to determine whether CCIS alters AsA synthesis, as measured by l-gulonolactone oxidase (GLO) activity, tissue AsA, lipid peroxides and tissue total antioxidant capacity (TAC). Stress was induced by dietary administration of corticosterone from 2 to 4 weeks of age and measurements were made at 0, 7 and 14 days post-treatment. Ascorbic acid synthesis was not influenced by CCIS but hepatic, cardiac, renal, bursal and duodenal AsA concentrations were significantly decreased and plasma TAC and uric acid concentrations were significantly elevated. Stress caused significant hepatomegaly and hepatic lipidosis but hepatic peroxides were not elevated despite the slight decrease in hepatic TAC. Tissue TAC varied in different organs. It was markedly elevated in the kidney, reduced by 49% in the spleen, and changes were not detected in the heart and duodenum even though AsA concentration was significantly decreased in all tissues. We conclude that CCIS caused a significant reduction in tissue AsA concentration but did not inhibit GLO activity. The change in AsA concentration was associated with increase, decrease or no change in TAC in tissues examined. The findings suggest that CCIS may alter AsA recycling, influx or turnover in different tissues of chickens.
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PMID:Effect of chronic oxidative/corticosterone-induced stress on ascorbic acid metabolism and total antioxidant capacity in chickens (Gallus gallus domesticus). 1761 8

This study was carried out to assess the influence of di(2-ethylhexyl)phthalate (DEHP) alone or associated with antioxidants on the male reproductive system in newborn rats, emphasizing the implications of oxidative stress and hormonal balance during prenatal and early postnatal periods. Wistar females were exposed by oral route to DEHP alone or associated with antioxidants from gestational day 7 to lactational day 2 according to the following treatment regimens: (C) vehicle control (canola oil + 1% Tween-80); (V) vitamin C (200 mg/kg) + canola oil; (R) resveratrol (10 mg/kg) + canola oil; (D) DEHP (500 mg/kg) + 1% Tween-80; (DV) DEHP (500 mg/kg) + vitamin C (200 mg/kg); and (DR) DEHP (500 mg/kg) + resveratrol (10 mg/kg). Two male pups per litter were randomly selected and necropsied on postnatal day 2. The brain and liver were removed and weighed and anogenital distance (AGD) was measured. Additionally, the testes were removed for assessment of intratesticular testosterone levels and histopathology; the liver was used to measure biomarkers of oxidative stress. Vitamin C and resveratrol alone did not affect the reproductive end points and did not induce oxidative stress. Exposure of dams to DEHP alone and associated with antioxidants resulted in hepatomegaly in offspring and significantly increased the incidence of multinucleated gonocytes in seminiferous cords. Testosterone and AGD presented a trend to decrease in DEHP-exposed groups. Catalase activity increased only in groups exposed to DEHP associated with antioxidants, although GST (gluthatione-S-transferase) activity decreased in all DEHP-exposed groups. The levels of hydroperoxides increased only in group exposed to DEHP associated with vitamin C. These results indicate that the association of DEHP with antioxidants was unable to ameliorate DEHP-induced reproductive changes, and the coadministration of DEHP and these antioxidants might even contribute to an overall increase in oxidative stress.
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PMID:Vitamin C and resveratrol supplementation to rat dams treated with di(2-ethylhexyl)phthalate: impact on reproductive and oxidative stress end points in male offspring. 1975 43