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:1.3.5.1 (
succinate dehydrogenase
)
8,177
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The possible role of Mg2+-HCO3-ATPase, carbonic anhydrase and several other enzymes in rat intestinal mucosa as mediators of the action of aldosterone has been examined. The small-intestinal tract was cut into seven segments, 15 cm each in length and the mucosa was scraped off, homogenized in 50 mM D-mannitol-2 mM Tris-HCl buffer (pH 7.1), differentially fractionated and a crude brush border was obtained. The mucosa from the colon and rectum was combined and used as the large-intestinal sample. Five days after the adrenalectomy, activities of brush border Mg2+-HCO3-ATPase and supernatant carbonic anhydrase from the upper small intestine decreased to about 60 and 40% of normal values, respectively. Activities of Na+-K+-ATPase, beta-glycerophosphatase and
succinate dehydrogenase
were all decreased. Two and 4 h after i.p. injection of aldosterone (40 micrograms/kg) to adrenalectomized rats, all enzyme activities increased except for Na+-K+-ATPase in the upper small intestine. In contrast, Mg2+-
HCO
-3-ATPase and carbonic anhydrase activities were unchanged 3 h after i.p. injection of dexamethasone (200 micrograms and 1 mg/kg). The activation of both Mg2+-HCO3-ATPase and carbonic anhydrase by a single injection of aldosterone was blocked by pretreatment with cycloheximide (1 mg/kg). These results suggest that aldosterone may induce the synthesis of enzyme proteins in the intestinal mucosa.
...
PMID:Brush border Mg2+-HCO-3-ATPase, supernatant carbonic anhydrase and other enzyme activities isolated from rat intestinal mucosa: effect of adrenalectomy and aldosterone administration. 613 8
In the hermaphroditic pulmonate snail Lymnaea stagnalis a blood-gonad (blood-testis) barrier appears to exist. Septate junctions between Sertoli cells and epithelial cells of the neck areas of the gonadal acini constitute this barrier; they separate the male from the female compartment. Experiments with tracer substances (colloidal gold particles, lanthanum nitrate, tannic acid) showed that the basal lamina around the acini hardly forms a barrier; only the larger colloidal gold particles do not pass this lamina. Physiological, the blood-gonad barrier is apparent in studies on the composition of gonadal fluid, which differs considerably from that of haemolymph. The osmolarity and the concentration of protein and amino acids in gonadal fluid exceed those of haemolymph. As to the major ions, in the gonadal fluid Na+ is partly replaced by K+, and
HCO
-3 is almost totally replaced by Cl-. Such a distribution of
HCO
-3 and Cl- is indicative of metabolic acidosis. The cytochemical localization of carbonic anhydrase activity in cells lining the acinar lumen (Sertoli cells, epithelial cells) suggests that these cells are involved in the process of ion exchange. The metabolic acidosis in the gonad might result from the anaerobic production of lactate and succinate by Sertoli cells; these cells lack the enzymes cytochrome oxidase, lactate dehydrogenase, and
succinate dehydrogenase
. Spermatogenic cells, on the other hand, do possess these enzymes. This probably indicates that these cells metabolize lactate and succinate secreted by Sertoli cells.
...
PMID:A morphological, enzyme-cytochemical, and physiological study of the blood-gonad barrier in the hermaphroditic snail Lymnaea stagnalis. 671 88
The question of whether elevated concentrations of CO
2
directly inhibit mitochondrial respiration in plants has received considerable attention. Although there is a growing consensus that elevated [CO
2
] rarely inhibits respiration of intact tissues, past studies have reported that elevated [CO
2
] does impact on O
2
uptake in isolated mitochondria; what remains unclear, however, is the site(s) where elevated [CO
2
] impacts on mitochondrial electron transport (ETC). Here we investigated direct effects of [CO
2
] on respiratory activity of ETC enzymes, intact mitochondria and whole tissues using potato tubers (Solanum tuberosum L. cv. Desiree). Plots of O
2
uptake against the redox poise of the ubiquinone (UQ) pool in isolated mitochondria were used to determine whether elevated [CO
2
] inhibits UQ-reducing and UQ-oxidising pathways differentially. Our results show that mitochondrial respiration was more inhibited via [CO
2
]/[
HCO
3
-
] effects on cytochrome c oxidase (COX) than on
succinate dehydrogenase
, with [
HCO
3
-
] rather than [CO
2
] inhibiting COX. However, the inhibitory effects at the mitochondrial level did not translate into inhibitory effects at the tissue level. Alternative oxidase (AOX) activity is normally absent in young potato tubers, as was the case in the present study. Thus, the lack of CO
2
-mediated inhibition at the tissue level was not the result of increases in AOX activity masking the effects of CO
2
elsewhere in the respiratory system. We discuss whether the direct impact of elevated [CO
2
] on respiration is dependent on the rate of metabolic activity and flux control coefficients in individual tissues.
...
PMID:Contrasting responses by respiration to elevated CO
2
in intact tissue and isolated mitochondria. 3268 37
