1939
DOI: 10.1001/archinte.1939.00180210153010
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Nephrosis Due to Carbon Tetrachloride

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1943
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Cited by 52 publications
(6 citation statements)
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“…Carbm tetrachloride impairs oxidative enzymes in liver microsomes by decreasing the amount of cytochrome 1 ) 4~ either due to an active metaholite (17) or free radical formation (18,191. Hepatotoxicity in rats is evident within 24 h of carbon tetrachloride treatment (1.0 mLkg) (8). However, the toxic effects of carhon tetrachloride to other organs such as the kidney do not occur until many hours to several days after the exposure to the toxin (20)(21)(22). Therefore, rats pretreated with carbon tetrachloride 24 h prior to study were used to ensure minimal damage to other organs.…”
Section: Discussionmentioning
confidence: 99%
“…Carbm tetrachloride impairs oxidative enzymes in liver microsomes by decreasing the amount of cytochrome 1 ) 4~ either due to an active metaholite (17) or free radical formation (18,191. Hepatotoxicity in rats is evident within 24 h of carbon tetrachloride treatment (1.0 mLkg) (8). However, the toxic effects of carhon tetrachloride to other organs such as the kidney do not occur until many hours to several days after the exposure to the toxin (20)(21)(22). Therefore, rats pretreated with carbon tetrachloride 24 h prior to study were used to ensure minimal damage to other organs.…”
Section: Discussionmentioning
confidence: 99%
“…Smetana (1) has shown that the distal tubule appears to bear the brunt of the renal pathological processes resulting in oliguria or anuria, and Woods (2) has demonstrated the identity of the renal pathology in this disease with that of the crush syndrome. This type of acute renal failure has therefore been included among the subclassifications of lower nephron nephrosis by Lucke (3).…”
mentioning
confidence: 99%
“…The enhanced CCL-induced hepatotoxicity after chronic pretreatment with alcohol has been ascribed to an increased metabolism of c c 1 4 to toxic intermediates (10) as a consequence of microsomal enzyme induction commonly observed after prolonged alcohol intake (13,14,15,16,17). Of particular interest was the clinical observation that the majority of patients with severe organic lesions due to ccI4 intoxication were heavy drinkers and had consumed alcohol shortly before, during or immediately after exposure to c c 1 4 (2, 3, 4, 5, 7,18,19,20,21,22,23).…”
mentioning
confidence: 99%