Detail of "115-20-8"

Reference

Inhibition of d-aminolevulinic acid dehydratase by trichloroethylene

Inhibition of d-aminolevulinic acid dehydratase by trichloroethylene. Koizumi, Akio; Fujita, Hiroyoshi; Sadamoto, Tetsuo; Yamamoto, Masayuki; Kumai, Miho; Ikeda, Masayuki (Sch. Med., Tohoku Univ., Sendai 980, Japan). Toxicology, 30(2), 93-102 (English) 1984. CODEN: TXCYAC. ISSN: 0300-483X. DOCUMENT TYPE: Journal CA Section: 4 (Toxicology) Male rats (8 animals/group) were exposed continuously to trichloroethylene (TRI) [79-01-6] for 48 or 240 h or methylchloroform (MC) [71-55-6] for 48 h at 50, 400, and 800 ppm. The inhibition of d-aminolevulinic acid dehydratase (ALA-D) [9036-37-7] was examd. in liver, blood, and bone marrow of naive and phenobarbital-pretreated animals exposed to TRI. A clear cut dose-effect relation between the exposure concn. or duration of exposure and the inhibition of ALA-D activity was seen for rats exposed to TRI. In addn. to this finding, significant interaction between TRI exposure and phenobarbital treatment was obsd. in the inhibition of ALA-D in liver and blood. MC did not produce inhibition. Trichloroacetic acid [76-03-9] and trichloroethanol [115-20-8] failed to inhibit the ALA-D activity in vitro. It seems that a metabolite(s) of TRI other than the above 2 substances may play a role in the inhibition of ALA-D. The inhibition of ALA-D (38 or 48% of the control in liver or blood, resp.) obsd. 9037-14-3 and 9036-37-7 which are cas registry numbers of substances are two of reagents here. after 240-h exposure at 400 ppm to TRI was accompanied by a significant elevation of d-aminolevulinic acid synthase [9037-14-3] (186% of the control) in liver and an increase in excretion of d-aminolevulinic acid [106-60-5] in urine (142% of the control). This occurred without an apparent wt. loss, liver injury, or hematol. changes. .

Dose-dependent induction and suppression of liver mixed-function oxidase system in chlorinated hydrocarbon solvent metabolism

Dose-dependent induction and suppression of liver mixed-function oxidase system in chlorinated hydrocarbon solvent metabolism. Koizumi, Akio; Kumai, Miho; Ikeda, Masayuki (Sch. Med., Tohoku Univ., Sendai 980, Japan). JAT, J. Appl. Toxicol., 3(4), 208-17 (English) 1983. CODEN: JJATDK. ISSN: 0260-437X. DOCUMENT TYPE: Journal CA Section: 4 (Toxicology) The effect of continuous exposure to trichloroethylene (TRI) [79-01-6], tetrachloroethylene (TETRA) [127-18-4], or methylchloroform (MC) [71-55-6] on the hepatic mixed-function oxidase system (MFOS) was studied in rats by using 10,000 ′ g supernatant fraction of liver. Exposure to TETRA for 240 h at 200, 100, and 50 ppm enhanced oxidative conversion of TETRA to trichloroacetic acid [76-03-9]. When the animals were exposed for 240 h to 200, 400, and 800 ppm, oxidative conversion of9MC to trichloroethanol [115-20-8] was elevated. However, elevation was less pronounced with the increase of exposure intensities from 400 to 800 ppm. With TRI, MFOS activities were more critically assessed as a function of duration and dose because the variable response in MFOS activity was obsd. in preliminary studies when rats were exposed to 400 ppm for 240 h. The MFOS activities in rats exposed to TRI at 50, 400, or 800 ppm for 48, 72, 168, and 240 h were measured. The MFOS activities were all suppressed after 48-h exposure irresp. of the exposure concn. After 72-240 h, suppression was superseded by activation at 50 ppm, while continuity of suppressive state was obsd. at 800 ppm and transitional state was the case of the exposure at 400 ppm. The possibility that epoxide hydratase would be involved in the metab. of TRI, but not in those of other 2 chem., was also presented. Based on these findings, math. models for TRI and TETRA metab. 71-55-6 and 76-03-9 are just another two chemicals used in this study. were established, which can explain hepatotoxicity appearing only after exposure to TRI at 800 ppm for 3168 h. .