Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038187 (starvation)
 24,951 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. Intracranial or subcutaneous doses of atropine or atropine methyl nitrate that were fully effective at preventing drinking in response to intracranial carbachol did not block angiotensin-induced drinking. 2. The nicotinic antagonist dihydro-beta-erythroidine given intracranially affected neither angiotensin- nor carbachol-induced drinking. 3. The dopaminergic antagonists haloperidol and spiroperidol injected intracranially blocked angiotensin-induced drinking but did not affect carbachol-induced drinking. 4. Angiotensin- and carbachol-induced drinking were unaffected by alpha- or beta-adrenergic antagonists except at toxic doses. 5. Destruction of catecholaminergic neurones with 6-hydroxydopamine markedly reduced angiotensin-induced drinking, but had relatively little effect on carbachol-induced drinking. 6. Intracranial haloperidol reduced the amount of water drunk in response to overnight deprivation of water, but did not affect feeding in response to overnight starvation or to intracranial noradrenaline. 7. Drinking following overnight water deprivation was unaffected by intracranial alpha- or beta-adrenergic antagonists. 8. Preventing dopaminergic transmission with intracranial haloperidol decreased the water to food ratio of the rat's intake after overnight starvation, whereas increasing the dopamine levels with the combination of FLA-63 and L-DOPA increased the ratio. 9. Intraventricular dopamine in large amounts caused the water-replete rat to drink. 10. It is concluded that among the many functions of dopaminergic systems in the brain is a role in the control of water intake, and that these systems participate in an important way in drinking in response to angiotensin.
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PMID:The relative importance of central nervous catecholaminergic and cholinergic mechanisms in drinking in response to antiotensin and other thirst stimuli. 24 Sep 34

To evaluate the specificity of some functional indices in assessment of body zinc nutrition status, we used experimental rat model to observe the effects of some factors, such as forced swimming, starvation, trauma and alcohol intoxication on zinc the status. Plasma zinc levels of rats significantly decreased after trauma increased after starvation. Liver zinc content showed a rising tendency in trauma and starvation rats. Activities of superoxide dismutase in red blood cells and alkaline phosphatase, mannosidase, 5'-nucleotidase in plasma of rats with alcohol intoxication declined significantly. Starvation led to decreased activities of alkaline phosphatase and angiotensin-converting enzyme, but increased activities of mannosidase. Trauma and forced swimming could cause increase of angiotensin-converting enzyme activity and decrease of 5'-nucleotidase activity, respectively. These results indicate that physiological and pathological effects should be excluded from of the above indices as plasma zinc index, in the assessment of body zinc nutrition status.
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PMID:[Effects of stress on indices for assessing zinc nutrition status]. 875 64

There is evidence to suggest that the mechanism of antioxidant effect of prostaglandin E1 (PGE1) is due to decrease of radical species generation by cytochrome P-450 in rat liver microsomes. Chronic alcohol intoxication increased NADPH oxidation, cytochrome P-450 content and NADPH-stimulated chemoluminiscence of microsomes. Ethanol also raised superoxide dismutase (SOD) activity in microsomes. PGE1 decreased cytochrome P-450 content, normalized NADPH oxidation, NADPH-induced chemoluminiscence and SOD activity in the liver of alcohol-treated rats. PGE developed the similar effect after microsomal induction by both acetone combined with starvation and phenobarbital normalizing all the above parameters. Therefore, PGE1 affects on both, ethanol-inducible IIE1 and phenobarbital-inducible IIB1 isoforms.
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PMID:Cytochrome P-450 and free radical generation in rat liver microsomes under the influence of prostaglandin E1. 887 71