Bromobenzene Metabolism and Hepatic Necrosis

Reid, Watson D.; Christie, B.G.B.; Krishna, Gopal; Mitchell, J. R.; Moskowitz, J.-P.; Brodie, Bernard B.

doi:10.1159/000136226

Cited by 133 publications

(33 citation statements)

References 4 publications

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“…Figure 1 shows *the variation of hepatic glutathione (GSH) concentration in rat liver as a function of the time of day. Food was withdrawn from animals at 4 PM, and groups of rats were sacrificed at 3 hr intervals. In a second experiment, a group of rats was fasted from 4 PM on day 1 and these animals were sacrificed beginning at 4 PM on day 2.…”

Section: Methodsmentioning

confidence: 99%

“…Food was withdrawn from animals at 4 PM, and groups of rats were sacrificed at 3 hr intervals. In a second experiment, a group of rats was fasted from 4 PM on day 1 and these animals were sacrificed beginning at 4 PM on day 2. The data show that GSH concentration, expressed as milligrams per 100 g of body weight, decreases precipitously after 4 PM in fed rats and reaches a minimum between 7 and 10 PM.…”

Section: Methodsmentioning

confidence: 99%

“…Other investigators (2) had reported a similar observation previously. Previous reports (3)(4)(5) had shown that glutathione was an important site of detoxification following exposure of rats to bromobenzene. From this, an initial hypothesis was developed which postulated glutathione as a site of detoxification of 1,1-DCE.…”

Section: Introductionmentioning

confidence: 96%

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Biochemical toxicology of unsaturated halogenated monomers.

Jaeger¹,

Conolly²,

Reynolds³

et al. 1975

Environ Health Perspect

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Previous inhalation toxicity studies from our laboratory have shown that 1,1-dichloroethylene (1,1-DCE), 1,1-dibromoethylene (1,1-DBE), and 2-chloro-1,3-butadiene (2-CBD) are more toxic to fasted rats than to fed rats. Vinyl chloride monomer (VCM) and 1,1-difluoroethylene (1,1-DFE) were not acutely hepatotoxic at 46,500 and 82,000 ppm, respectively, in normal male rats, whether fed or fasted. On a molar basis, 1,1-DBE and 1,1-DCE have similar toxicities while 2-CBD is less toxic. All three compounds produce similar elevation of serum transaminase and bloody ascites, although at differing times following differing exposure concentrations.1,1-DCE produces massive midzonal hepatic necrosis with hepatic thrombosis and chromatolysis within 2 hr after a 4 hr exposure of fasted rats to 200 ppm. Subsequent to formation of this midzonal lesion, the central portion of the lobule collapses, accompanied by congestion, ascites, and an increased hematocrit in the rat. Serum transaminase and sorbital dehydrogenase are greatly elevated at 6 hr. This effect in fasted rats is associated with glutathione (GSH) depletion. Diethyl maleate (DEM) which depletes GSH in fed rats potentiates the injury associated with 1,1-DCE exposure as well as that produced by 2-CBD. Rats fed ad libitum and exposed to 1,1-DCE or 2-CBD at night, a time of low hepatic GSH concentration, exhibit enhancement of hepatotoxic response when compared to animals exposed during the day when GSH is high.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

See 1 more Smart Citation

Biochemical toxicology of unsaturated halogenated monomers.

Jaeger¹,

Conolly²,

Reynolds³

et al. 1975

Environ Health Perspect

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“…'.e et al, 1985;Reid et al, 1973;Brodie et al, 1971;Reid et al, 1971). Since chlor3benzene, bromobenz3ne…”

Section: Halocarbon Occurrence and Usementioning

confidence: 99%

Mechanisms of Halocarbon-Induced Hepatotoxicity in the Mouse

Smith¹,

Gandy²

1990

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“…1), 일부는 epoxide hydrolase에 의해 무독화 되는 것으로 보고되고 있다 (Heijine et al, 2004). 한편, bromobenzene의 중간 대사산물인 bromobenzene-3,4-oxide는 친전자성 물질로 신속하게 무독화 되지 않으면 생체내의 친핵 성 물질로 알려져 있는 DNA, RNA, 단백질 및 지질 등과 같은 물질과 결합하여 조직의 손상을 유발시키는 것으로 잘 알려져 있다 (Reid et al, 1971). 이와 같은 bromobenzene의 대사는 혈청 중 Aminotransferase (AST, ALT) 측정 Reitman and Frankel (1957)의 방법에 준하여 조제된 kit (Asan Pharmaceutical)를 사용하여 alanine transaminase (100 mL 당 DL-alanine 1,780 mg 및 α-ketoglutamic acid 29.2 mg 함유), aspartate transaminase (100 mL 당 L-aspartic acid 2,660 mg 및 α-ketoglutamic acid 29.2 mg함유) 기질액 1.0 mL를 37℃ 에서 5분간 preincubation 시킨 후 혈청 0.2 mL를 넣어 37℃에서 alanine transami-nase는 30분, aspartate transaminase 는 60분간 반응 시킨 후 정색시액 (2,4-dinitrophenylhydrazine, 19.8 mg/100 mL 함유) 1.0 mL를 첨가하고 0.4 N-NaOH 용액 1.0 mL를 가하여 혼합한 후 10분간 실온에서 방치하고 파장 505 nm에서 흡광도를 측정하여 활성도를 표준검량선에 준하 여 혈청 mL당 Karmen (1955) unit로 표시하였다.…”

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Hepatic Detoxification and Antioxidant Activity in Sea-urchin Roe and Ethanol Extract of Roe

Lee¹,

Ha²,

Choi³

et al. 2010

Korean Journal of Fisheries and Aquatic Sciences

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Sea-urchins (Anthocidaris crassispina) are widely distributed in the East Sea of Korea. The aim of this study was to evaluate the hepatoprotective effects of sea-urchin roe on bromobenzene (BB)-induced liver damage in rats. The antioxidative and detoxifying properties of sea-urchin roe in BB-poisoned rat liver was examined by chemical analysis of serum aminotransferase (AST, ALT), glutathione S-transferase (GST), γ-glutamylcystein synthetase, glutathione reductase, epoxide hydrolase, amino-N-demethylase (AD), aniline hydrolase (AH) enzyme activity, as well as lipid peroxide and glutathione contents. Sea-urchin roe inhibited the increase of serum AST, ALT enzyme activity. Increasing lipid peroxide contents and AD and AH activities were significantly decreased in ethanol extract of sea-urchin roe. GST, γ-glutamylcystein synthetase, glutathione reductase and epoxide hydrolase enzyme activities increased in sea-urchin roe-fed group, compared with the BB-treated group. These results suggest that sea-urchin roe facilitates recovery from liver damage by enhancing antioxidative defense mechanisms and hepatic detoxication metabolism.

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Bromobenzene Metabolism and Hepatic Necrosis

Cited by 133 publications

References 4 publications

Biochemical toxicology of unsaturated halogenated monomers.

Biochemical toxicology of unsaturated halogenated monomers.

Mechanisms of Halocarbon-Induced Hepatotoxicity in the Mouse

Hepatic Detoxification and Antioxidant Activity in Sea-urchin Roe and Ethanol Extract of Roe

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