Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.3.5.1 (succinate dehydrogenase)
 8,177 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The differentiation of perirenal adipose tissue was ascertained in fetuses from Ossabaw (wild and obese) and cross-bred lean dams at 70, 90 and 110 days gestation and from domestic lean and obese dams (USDA) at 110 days gestation. Condensation of presumptive adipocyte clusters was more apparent in Ossabaw sections than in cross-bred (lean) sections at 90 and 110 days gestation. Enzyme and lipid histochemistry showed fat cell cluster development to be largely independent of fetal strain (Ossabaw vs crossbred). However, adipocytes in Ossabaw fetuses were larger (110 days) and more reactive for esterase activity (all three ages) than were adipocytes from crossbred fetuses. Fetuses from USDA-obese dams had larger fat cell diameters (P less than 0.01), a higher percentage of lipoprotein lipase (LPL) positive cells than did fetuses from USDA-lean dams. Perirenal fat pad weights, percent depot lipid, percentages of glucose-6-phosphate dehydrogenase (G6PDH) and succinate dehydrogenase (SDH) positive cells were independent of fetal strain (USDA, lean vs obese). Fat cell cluster development was independent of fetal strain but large cellular condensations of presumptive cells were only present in sections from lean fetuses. Immature capillary beds (devoid of adipocytes) were demonstrable in lean sections but were not observed in obese sections. Morphological and histochemical results from both studies provide no evidence for brown adipocyte-like cells in fetal perirenal tissues.
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PMID:The development of perirenal fat depots in obese and lean pig fetuses. 342 14

Concurrent administration of a high dose of gentamicin (GM; 125mg/kg IM) and ethacrynic acid (EA; 40mg/kg IV) results in rapid destruction of virtually all cochlear hair cells; however, the cell death signaling pathways underlying this rapid form of hair-cell degeneration are unclear. To elucidate the mechanisms underlying GM/EA-mediated cell death, several key cell death markers were assessed in the chinchilla cochlea during the early stages of degeneration. In the middle and basal turns of the cochlea, massive hair-cell loss including destruction of the stereocilia and cuticular plate occurred 12h after GM/EA treatment. Condensation and fragmentation of outer hair-cell nuclei, morphological features of apoptosis, were first observed 5-6h post-treatment in the basal turn of the cochlea. Metabolic function, reflected by succinate dehydrogenase histochemistry and mitochondrial staining, decreased significantly in the basal turn 4h following GM/EA treatment; these early changes were accompanied by the release of cytochrome c from the mitochondria into the cytosol and intense expression of initiator caspase-9 and effector caspase-3. GM/EA failed to induce expression of extrinsic initiator caspase-8. These results suggest that the rapid loss of hair cells following GM/EA treatment involves cell death pathways mediated by mitochondrial dysfunction leading to the release of cytochrome c, activation of initiator caspase-9 and effector caspase-3.
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PMID:Mechanisms of rapid sensory hair-cell death following co-administration of gentamicin and ethacrynic acid. 1971 47