Detail of "1838-59-1"

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Histopathological study on experimental liver cirrhosis induced by allyl formate

Histopathological study on experimental liver cirrhosis induced by allyl formate. Nakatani, Toshio (Dep. Pathol., Wakayama Med. Coll.Chemical with cas number 1838-59-1 also plays role., Wakayama, Japan). Wakayama Med. Rep., 19(2-3), 99-120 (English) 1976. CODEN: WKMRAH. DOCUMENT TYPE: Journal CA Section: 14 (Mammalian Pathological Biochemistry) Exptl. liver cirrhosis induced by allyl formate was studied in Wistar rats. Serial changes from periportal cell damage to portal fibrosis to liver cirrhosis were seen. Periportal hepatocytes showed morphol. and functional changes in rough endoplasmic reticulum, mitochondria, and bile canaliculi. It is suggested that proliferated bile ductules, mast cells, fibroblasts, myofibroblasts, and fat-storing cells might be related to hepatic fibrogenesis. Small liver cell adenomas were also seen in 4 of 74 rat livers (5.4%) with fibrosis or cirrhosis, but no malignancy was seen. .

Effects of hepatotoxicants on the induction of microsomal monooxygenase activity in sunfish liver by b-naphthoflavone and benzo[a]pyrene

Effects of hepatotoxicants on the induction of microsomal monooxygenase activity in sunfish liver by b-naphthoflavone and benzo[a]pyrene. Oikari, Aimo; Jimenez, Braulio (Dep. Biol., Univ. Joensuu, Joensuu SF-80101, Finland). Ecotoxicol. Environ. Saf., 23(1), 89-102 (English) 1992. CODEN: EESADV. ISSN: 0147-6513. DOCUMENT TYPE: Journal CA Section: 4 (Toxicology) Effects of chem. induced hepatic injury on biotransformation enzymes in fish were studied. Sunfish hybrids Lepomis macrochirus ′ L. cyanellus) were dosed per os with allyl formate (ALF) and CCl4, and the induction of liver EROD (7-ethoxyresorufin O-deethylase) activity was subsequently challenged by injections of b-naphthoflavone (BNF) and benzo[a]pyrene (B[a]P). Hepatotoxicity of chem. treatments was assessed using blood enzymes ASAT, ALAT, and LDH) along with other biochem. variables. Both hepatotoxicants partially abolished the induction of EROD (maximally by 76-89%), and the decrease in induction was dose related. The cytosolic activity of glutathione S-transferase (GST) in the liver decreased in parallel with the decrease in EROD induction. Fish receiving high doses of ALF exhibited significantly less microsomal and blood plasma proteins and, occasionally, were jaundiced. These symptoms, however, were less sensitive indicatwrs of hepatotoxicity than alterations in liver EROD and GST. ALF and CCl4 increased the activities of hepatic enzymes in the blood plasma, indicating cytotoxicity. In addn. B[a]P, unlike BNF, also increased plasma activities of LDH and ALAT at a dose inducing liver EROD, implying simultaneous hepatotoxicity at high sublethal levels of this xenobiotic. Therefore, hepatotoxic chems. absorbed by fish may act antagonistically by decreasing the degree of induction of the cytochrome P 450 system relative to the inherent capacity of inducing xenobiotic chems. present in the environment. When assessing the toxicol. 1838-59-1 and 50-32-8 are just another two chemicals used in this study. status of water using fish health biomarkers, it is advisable to measure a concert of metabolic and biochem. variables instead of any single biomarker. .