Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A quantitative animal model was developed to study amelioration of carbon tetrachloride-induced hepatic injury by post-toxicant administration of cystamine. Amelioration of CCl4-induced injury by post-toxicant cystamine treatment was compared to prevention of injury by cystamine pretreatment and possible mechanisms of the post-toxicant cytoprotective effect were investigated. Pretreatment of rats with cystamine dihydrochloride (300 mg/kg, p.o.) 30 min prior to CCl4 (0.25 ml/kg, i.p.) prevented CCl4-induced hepatic necrosis, plasma enzyme elevations, and hepatic calcium accumulation. When administered up to 12 h after CCl4, a single oral dose of cystamine inhibited necrosis in a dose-dependent manner, but did not reduce CCl4-induced plasma enzyme elevation or hepatic calcium accumulation. Cystamine post-treatment, therefore, does not appear to inhibit toxicant-induced influx of extracellular calcium into toxicant-damaged cells. This also suggests that the influx of extracellular calcium does not necessarily constitute an irreversible event leading to cell death. The mild hypothermia induced by post-toxicant treatment with cystamine did not delay the appearance of the lesion. Evidence for a slightly earlier regeneration of hepatic tissue was noted when cystamine was administered 12 h after CCl4. However, this effect was observed too long after exposure to the toxicant to account for the protection from necrosis observed 24 h after CCl4.
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PMID:Amelioration of carbon tetrachloride-induced hepatic necrosis by post-toxicant treatment with cystamine. 370 80

Oral administration of diethyldithiocarbamate (DTC) and carbon disulfide (CS2) protected mice against CHCl3-induced kidney injury, as evidenced by normalization of delayed plasma phenolsulfonphthalein clearance, suppression of increased kidney calcium content and prevention of renal tubular necrosis. In CCl4-treated mice, in which liver microsomal monooxygenase activities were decreased markedly, and kidney microsomal aniline hydroxylase and p-nitroanisole demethylase activities were increased to about twice those of the untreated mice, renal toxicity of CHCl3 was greatly potentiated, and the latter effect was also blocked by both agents. DTC and CS2 per se markedly decreased kidney microsomal aniline hydroxylase and p-nitroanisole demethylase activities at 1 hr after oral administration, accompanying a moderate loss of cytochrome P-450 content, in both normal and CCl4-treated mice. The protection was not due to hypothermia, because pretreatment with DTC or CS2 (p.o.) also prevented the hypothermia induced by CHCl3. The mechanism of the protection may have involved inhibition of metabolic activation of CHCl3 in the kidney rather than in the liver.
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PMID:Protective action of diethyldithiocarbamate and carbon disulfide against renal injury induced by chloroform in mice. 631 19

Bilirubin is a sensitive marker of toxic liver injury. Carbontetrachloride (CCl4) is used in some manufactures and laboratories. An acute intoxication is a peril. We have performed experiments to state total, indirect and direct bilirubin levels in rats exposed to a single CCl4 dose of 1.25 ml/kg. Total bilirubin in normal rats is 3.13 +/- 0.13 mumol/l. 58.6% is direct conjugated and 41.3% indirect unconjugated bilirubin. One hour after CCl4 administration bilirubin started to increase and reached its peak in the second hour. 24 h later a decrease began but even 72 h after intoxication it was not normalized. Ursodesoxycholic acid (UDCA, CAS 128-13-2, Ursofalk) treatment (25 mg/kg/dose) lowered bilirubin, returning to normal level 24 h after CCl4 administration. Hypothermia aggravates intoxications. In CCl4 lesion it develops 1 h after exposure. UDCA has not influenced low body temperature but liver function, conjugating capacity was restored. In CCl4 poisoning it is suggested to start UDCA treatment as early as possible and to continue it for some more days after improvement of serum bilirubin concentration.
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PMID:Studies on the effect of ursodesoxycholic acid on rats with acute carbontetrachloride injury. 920 82