Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.12.7.2 (hydrogenase)
 3,522 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have examined the effect of recent onset diabetes on several aspects of hepatic microsomal metabolism in both streptozotocin (STZ)-induced and spontaneously diabetic BioBreeding (BB) male and female Wistar rats. Differential alterations of the diabetic state on hepatic microsomal enzyme activities were observed. Female diabetic rats exhibited no change in benzo [a]pyrene (BP) hydroxylase activity, a decrease in testosterone delta 4-hydrogenase, and an increase in aniline hydroxylase. On the other hand, male diabetic rats demonstrated a decrease in hepatic BP hydroxylase activity, no change in testosterone delta 4-hydrogenase, and an increase in aniline hydroxylase. Insulin treatment corrected these effects. No change in kidney BP hydroxylase activity was apparent in either female or male diabetics. There were no marked differences between the chemically induced and genetic models of diabetes with respect to the metabolism studies. Serum testosterone levels were significantly lower than control in male BB diabetics, whereas no change was apparent in female diabetics. Light microscopy and serum insulin determinations indicated that the spontaneously diabetic animals we examined were not severely diabetic. From electrophoresis of hepatic microsomal proteins we determined that spontaneous diabetes of short duration does alter the protein distribution in the cytochrome P-450 region. We conclude that the acute effects of STZ-induced and spontaneous diabetes on hepatic microsomal metabolism are quantitatively and qualitatively similar, despite probable differences in etiology of the diabetic state.
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PMID:Differential effects of diabetes on microsomal metabolism of various substrates. Comparison of streptozotocin and spontaneously diabetic Wistar rats. 634 6

Age-related changes in heme and hemoproteins, as well as the effect of testosterone treatment on these modifications were examined in male Sprague-Dawley rats. The activity of delta-aminolevulinic acid synthase (ALA-S) and the microsomal concentration of heme in aged rats were decreased by 37% and 33%, respectively, as compared to young values. In contrast, a marked increase in the activity of microsomal heme oxygenase (MHO) was seen in these animals. In aged rats, the level of cytochrome P-450 was decreased by 37%, as compared to young values. Furthermore, the activities of benzo[a]pyrene hydroxylase and aniline hydroxylase were decreased in proportion to the microsomal content of cytocyrome P-450. Steroid delta 4-hydrogenase, an index of endogenous substrate metabolism, exhibited no changes in activity during the aging process. The level of various hemoproteins such as cytochrome b5 and tryptophan pyrrolase in aged animals remained unaltered despite the decreased hepatic concentration of heme. It is worth noting that testosterone treatment of aged castrated rats restored the level of heme and cytochrome P-450 and the altered enzymatic activities of ALA-S and MHO to the "young" condition. In view of these findings, it is concluded that the events which lead to the low level of heme and cytochrome P-450 and its dependent mixed function oxidase activity during the senescent period could be due to increased rates of MHO and diminished ALA-S activities in these animals.
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PMID:Modification of age-induced changes in heme and hemoproteins by testosterone in male rats. 665 12

Previous studies have established that the effects of estradiol (E2) on hepatic steroid and drug metabolism are demonstrable only in the presence of the pituitary gland. Studies were carried out to test the hypothesis that GH is the pituitary feminizing factor mediating the actions of E2 on hepatic metabolism. E2 and GH administered to castrated male rats had similar effects on hepatic enzymes, decreasing the oxidataive metabolism of drugs [ethylmorphine demethylation, aniline, hydroxylation, and benzo(a)pyrene hydroxylation) and increasing steroid (corticosterone) delta 4-hydrogenase activity. None of these effects of E2 or GH could be demonstrated in hypophysectomized (hypox) rats. However, GH administration to T4- or ACTH-treated hypox rats resulted in some of the changes in drug and steroid metabolism seen in animals with intact pituitary glands. The actions of GH on hepatic microsomal enzymes were fully demonstrable in hypox rats receiving both T4 and ACTH. E2 had no effects in T4 plus ACTH-treated hypox rats. These and prior observations are consistent with the hypothesis that GH mediates the actions of E2 on hepatic microsomal drug- and steroid-metabolizing enzymes. The data also indicates that the cations of GH on hepatic metabolism are dependent upon the interactions with still other endocrine factors.
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PMID:Is growth hormone the pituitary feminizing factor mediating the actions of estradiol on hepatic drug and steroid metabolism? 677 28

Male inbred Fischer rats were fed a diet containing 5 p.p.m. aflatoxin for 1, 3, 4 1/2 and 6 weeks at which times groups were killed for histological and histochemical study. Aflatoxin produced a scattered individual cell necrosis of parenchymal cells by 1 week. At 3 weeks small basophilic proliferative foci were seen which increased in size and abundance to 6 weeks. These foci showed starvation-resistant glycogen, variable depletion of glucose-6-phosphatase, succinic dehydrogenase, aniline hydrogenase, membrane ATPase and acid phosphatase. At 6 weeks the foci showed the presence of gamma glutamyl transpeptidase and glucose-6-phosphate dehydrogenase. The basophilic foci were not preceded by other focal histological and histochemical change. The basophilic proliferative lesions are observed when an irreversible change has been induced in the liver. The role of such lesions in the histogenesis of hepatocellular carcinoma is discussed.
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PMID:Histochemical studies on the early proliferative lesion induced in the rat liver by aflatoxin. 724 Dec 69