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 sublethal effect of
naphthalene
was studied on the physiology of a mud crab Scylla serrata. The 96 h acute toxicity of
naphthalene
was determined and found to be 28 mg 1(-1) (LC100), 18 mg 1(-1) (LC50), 10 mg 1(-1) (LC0) respectively. The 30 days sublethal effect (LC0) 9 mg 1(-1), 8 mg 1(-1), 10 mg 1(-1), of
naphthalene
was investigated in the crab S. serrata with reference to oxygen consumption and changes in the activity of respiratory enzymes. The results indicated that
naphthalene
caused disturbance in the normal physiology of the crab. The bioaccumulation of
naphthalene
was also investigated in gills, hepatopancreas, haemolymph and ovary. The consumption of oxygen increased in the
naphthalene
medium when compared with that of the crabs exposed to
naphthalene
free medium. A decreased trend in the activity of respiratory enzymes such as lactate dehydrogenase (LDH), isocitrate dehydrogenase (ICDH),
succinate dehydrogenase
(
SDH
), malate dehydrogenase (MDH), alpha-ketoglutarate dehydrogenase (alpha-KDH) and glutathione (GSH) were recorded in the hepatopancreas, ovary and gills of S. serrata for all the tested concentrations of
naphthalene
and the results were analyzed for their significance.
...
PMID:Changes in oxygen consumption and respiratory enzymes as stress indicators in an estuarine edible crab Scylla serrata exposed to naphthalene. 1628 45
Rhizophora apiculata bark extract was tested for its free radical scavenging activity and protective role against mitochondrial dysfunction in
naphthalene
stressed rats. Lipid peroxidation activity was increased and activity of mitochondrial enzymes (cytochrome-c-oxidase, NADH-dehydrogenase, alpha-ketoglutarate dehydrogenase and
succinate dehydrogenase
) and glutathione was decreased in the liver and kidney of rats intoxicated with
naphthalene
when compared to control rats. Intraperitoneal administration of plant extract significantly reduced the lipid peroxidation, increased the activity of mitochondrial enzymes and increased glutathione to near control levels. These results suggest that the sulfated polysaccharides in R. apiculata play a protective role through their free radical scavenging properties.
...
PMID:Free radical scavenging activity of the marine mangrove Rhizophora apiculata bark extract with reference to naphthalene induced mitochondrial dysfunction. 1686 Jul 84
Endogenous striatal dopamine (DA) overflow has been associated with neuropathological conditions resulting from ischemia, psychostimulants, and metabolic inhibition. Malonate, a reversible inhibitor of
succinate dehydrogenase
, models the effects of energy impairment in neurodegenerative disorders. We have previously reported that the striatal DA efflux and damage to DA nerve terminals resulting from intrastriatal malonate infusions is prevented by prior DA depletion, suggesting that DA plays a role in the neuronal damage. We presently report that the malonate-induced DA efflux is partially mediated by reverse transport of DA from the cytosol to the extracellular space via the DA transporter (DAT). Pharmacological blockade of the DAT with a series of structurally different inhibitors [cocaine, mazindol, 1-(2-(bis(4-fluophenyl methoxy) ethyl)-4-(3-(4-fluorophenyl)-propyl)piperazine) dimethane sulfonate (GBR 13098) and methyl(-)-3beta-(p-fluorophenyl)-1alphaH,5alphaH-tropane-2beta-carboxylate1,5-
naphthalene
(Win 35,428)] attenuated malonate-induced DA overflow in vivo and protected mice against subsequent damage to DA nerve terminals. Consistent with these findings, the DAT inhibitors prevented malonate-induced damage to DA neurons in mesencephalic cultures and also protected against the loss of GABA neurons in this system. The DAT inhibitors did not modify malonate-induced formation of reactive oxygen species or lactate production, indicating that the DAT inhibitors neither exert antioxidant effects nor interfere with the actions of malonate. Taken together, these findings provide direct evidence that mitochondrial impairment and metabolic stress cause striatal DA efflux via the DAT and suggest that disruptions in DA homeostasis resulting from energy impairment may contribute to the pathogenesis of neurodegenerative diseases.
...
PMID:Mitochondrial stress-induced dopamine efflux and neuronal damage by malonate involves the dopamine transporter. 1709 Jul 4
