Protective effect of flavonoids from Cyclocarya paliurus leaves against carbon tetrachloride-induced acute liver injury in mice
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CARBON TETRACHLORIDE POISONING
Protection from carbon tetrachloride (CCL4)-induced hepatotoxicity by protein A was assessed histologically in rats. Carbon tetrachloride exposure produced swollen, vacuolated and necrotic cells in the centrilobular region of the hepatocyte in rats. Animals given protein A prior to and during CCL1 treatment showed a complete absence of hepatic lesions. Our study showed that protein A, a potent immunomodulator, has the potential to reduce liver injury caused by carbon tetrachloride, a known hepatotoxin in the rat.
Hepatotoxin
CARBON TETRACHLORIDE POISONING
CCL4
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Case histories of twelve patients treated for carbon tetrachloride poisoning at the Toxicological Clinic, Institute of Internal Medicine, Medical Academy of Cracow, during 1971-1975, ware analysed retrospectively. All patients were found to have developed some liver damage, two of them exhibiting acute renal failure, another two--impaired central nervous system. Nine of the patients developed changes indicative of adverse effects of carbon tetrachloride upon the cardiac muscle.
CARBON TETRACHLORIDE POISONING
Liver damage
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CCL4
Lipid peroxide
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Hepatotoxin
CARBON TETRACHLORIDE POISONING
Liver function
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CARBON TETRACHLORIDE POISONING
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CARBON TETRACHLORIDE POISONING
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Abstract Three cases of poisoning by carbon tetrachloride in the one industry are reported. Liver damage as evidenced by altered liver function tests was a feature of other workmen of this plant also exposed to carbon tetrachloride. Kidney damage, which is a feature of other reported cases of carbon tetrachloride poisoning, was only shown by one of the cases reported here. The dangers of carbon tetrachloride are noted, and care in its industrial and household use emphasized.
CARBON TETRACHLORIDE POISONING
Carbon fibers
Tetrachloride
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CARBON TETRACHLORIDE POISONING
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Microsomes from livers of albino rats treated with carbon tetrachloride were compared with those from normal rats with respect to their ability to incorporate amino acid. Acute carbon tetrachloride poisoning results in depressed capacity of microsomes to incorporate amino acid. From ultracentrifugal data, there is an apparent dissociation of 79S ribosomes into 54S components.
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Administration of sulfanila-mide to rats retards the development of liver cirrhosis from chronic poisoning with carbon tetrachloride. A number of vitamins and amino acids were tested for possible protective action in acute poisoning experiments, but none was found to increase the animal's tolerance. Administration of para-amino-benzoic acid did not inhibit the protective action of sulfanilamide against acute poisoning by carbon tetrachloride.
Sulfanilamide
CARBON TETRACHLORIDE POISONING
Liver damage
CCL4
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