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

The experiments carried out for the study aimed at determining the prenatal sensitivity to cadmium in the aspect of beth morphological and functional condition of placenta. The experiments were carried out on 80 pregnant female rats divided into three experimental groups and a control one. The experimental animals were daily administered, intragastrically, aqueous solution of cadmium chloride, from the 7th to the 19th day of pregnancy, in doses differing between the experimental groups: 2, 10 and 22 mg of CdCl2 per kilogram of body weight, respectively. The animals were decapitated on the 21st day of pregnancy. Placenta sections, besides hematoxylin and eosin staining, were examined for the activity of the following enzymes: succinic dehydrogenase (SDH) E.C.1.3.99.1., lactate dehydrogenase (LDH) E.C.1.1.1.27., NADH-tetrazole reductase (NADH-t.r.), without a catalog number, and their glycogen reaction was checked. The results of the experiments proved cadmium chloride to cause considerable damage to the enzymatic apparatus of placenta, leading to energy deficit in the cells of both the fetal and the maternal part of this organ. The multienzymatic changes observed preceded the morphologic ones by far.
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PMID:[Dynamics of morphological and cytochemical changes in the placenta following cadmium chloride intoxication]. 130 26

The utilization of cholesterol for steroid hormone synthesis by human placental mitochondria is poorly understood. The human placenta does not express the steroidogenic acute regulator protein, which is critical for cholesterol delivery to the cholesterol side chain cleavage system in adrenal and gonadal mitochondria. We explored the mechanism underlying cholesterol transport in human placental mitochondria by measuring its transformation into pregnenolone. Mitochondria of syncytiotrophoblast from human term placenta were isolated by centrifugation through a sucrose gradient. The synthesis of pregnenolone in the presence of exogenous cholesterol was increased two-fold in syncytiotrophoblast mitochondria. Treatment of mitochondria with trypsin prevented the increase in the synthesis of pregnenolone in the presence of exogenous cholesterol. However, when 22-OH cholesterol, a substrate that readily crosses membranes, was added, the trypsin-treated mitochondria synthesized increased amounts of pregnenolone. The trypsin-treated mitochondria were intact, since oxygen consumption, succinate dehydrogenase and the adenine nucleotide translocase activities were not significantly different from in untreated mitochondria. However, activity of NADH cytochrome c oxidoreductase, an outer mitochondrial membrane enzyme, was reduced in the trypsin-treated mitochondria, reflecting the selective degradation of proteins. In addition, SDS-PAGE analysis revealed the loss of a prominent 34 kDa band which proved to be a novel porin-like protein that binds to cholesterol. These results support our previous assumption that human placental mitochondria employ a novel protein(s)-mediated the mechanism to take up cholesterol for steroidogenesis.
Placenta 2000 Sep
PMID:A trypsin-sensitive protein is required for utilization of exogenous cholesterol for pregnenolone synthesis by placental mitochondria. 1098 68

Mitochondrial respiratory chain enzyme Complexes are present in placenta at proportion similar to other tissues with exception of glycerophosphate dehydrogenase (mGPDH) which is expressed at a very high rate. As shown by Western blot quantification and respiratory chain enzyme activity measurements, the specific content of mGPDH is similar to that of succinate dehydrogenase or NADH dehydrogenase. Using fluorometric probe dichlorodihydrofluorescein diacetate we found that placental mitochondria display high rate of glycerophosphate-dependent hydrogen peroxide production. This was confirmed by oxygraphic detection of glycerophosphate-induced, KCN- or antimycin A-insensitive oxygen uptake. Hydrogen peroxide production by mGPDH was highly activated by one-electron acceptor, potassium ferricyanide and it was depressed by inhibitors of mGPDH and by cytochrome c. Our results indicate that mGPDH should be considered as an additional source of reactive oxygen species participating in induction of oxidative stress in placenta.
Placenta
PMID:Specific properties of heavy fraction of mitochondria from human-term placenta - glycerophosphate-dependent hydrogen peroxide production. 1594 44