Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: EC:1.9.3.1 (
cytochrome oxidase
)
8,822
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
[4-14C]
Cholesterol
side chain cleavage, progesterone synthesis, and
cytochrome oxidase
activities were measured in mitochondria from unincubated and short term incubated large (8-10 mm) follicles isolated from porcine ovaries. Compared to the activity of mitochondria from unincubated follicles, specific [4-14C]cholesterol side chain cleavage activity in mitochondria from follicles incubated with LH (0.05 microgrogram/ml) did not change significantly after 12 h, but increased almost 2-fold after 18 h and 5-fold after 24 h. Also, specific mitochondrial progesterone synthesis activity increased dramatically after incubation of follicles for 24 h with LH. In comparison, mitochondria prepared from follicles incubated without LH showed no significant change in specific [4-14C]cholesterol side chain cleavage or progesterone synthesis activities after 18 h of incubation. While both of these activities increased after incubating follicles 24 h without LH, the values were significantly lower than those observed for preparations from follicles incubated with LH. In contrast to these changes in mitochondrial steroidogenesis, specific
cytochrome oxidase
activity in mitochondria did not change after incubation of follicles without or with LH. It is concluded that incubation of follicles with LH stimulates the development of mitochondrial steroidogenesis but initially does not affect some components of the respiratory chain.
...
PMID:Increases in mitochondrial steroidogenesis after short term incubation of porcine ovarian follicles with luteinizing hormone. 43 36
Monkeys (Macaca nemestrina) were divided into four groups, and each group was fed a particular diet. The variables in the diets were as follows: diet A, 0.3 mg cholesterol/kcal nutrient; diet B, 1.0 mg cholesterol/kcal nutrient; diet C, 0.3 mg cholesterol/kcal nutrient, ethanol (36% of calories); diet D, 1.0 mg cholesterol/kcal nutrient, ethanol (36% of calories). Monkeys on the diets containing ethanol developed fatty liver. Mitochondria from ethanol-fed animals demonstrated significant decreases in uncoupler-stimulated, state 3, and state 4 succinate oxidation activity; respiratory control ratio; and ATP content. Liver microsomes isolated from the ethanol-fed groups demonstrated increased ethanol oxidizing activity with either NADPH or H2O2 as cosubstrate. Aniline hydroxylase and aminopyrine-N-demethylase activities were also elevated in ethanol-fed animals. The alterations in these functional properties were related primarily to ethanol in the diets.
Cholesterol
, while being less of a perturbant than ethanol, did elicit a significant decrease in
cytochrome oxidase
activity of mitochondria and a small but statistically significant increase in microsomal-associated ethanol oxidation activity. It appeared to potentiate the effect of ethanol in lowering mitochondrial respiratory control and ATP concentrations.
...
PMID:Effect of dietary ethanol and cholesterol on metabolic functions of hepatic mitochondria and microsomes from the monkey, Macaca nemestrina. 702 93