Oxidative Dealkylation of Tetra-, Tri-, and Dialkyltins and Tetra- and Trialkylleads by Liver Microsomes.

Casida, John E.; Kimmel, Ella C.; Holm, Beryl; Widmark, Gunnar; Koskikallio, Jouko; Kachi, Sukeji

doi:10.3891/acta.chem.scand.25-1497

Cited by 56 publications

(13 citation statements)

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“…The metabolism of the butyltin compounds by cytochrome P450 enzymes has been suggested to play an important role in the induction of biological effects; tributyltin was found to undergo hydroxylation followed by dealkylation to produce dibutyltin, monobutyltin and inorganic compounds in the presence of microsomes and NADPH in vitro (Casida et al 1971;Fish 1984;Fish et al 1976;Kimmel et al 1977). Moreover, several studies have shown that a variety of metabolites are formed in rat (Matsuda et al 1993) and mouse liver (Ueno et al 1997) during the metabolism of TBTC in vivo.…”

Section: Introductionmentioning

confidence: 96%

Comparison of hepatotoxicity and metabolism of butyltin compounds in the liver of mice, rats and guinea pigs

et al. 2003

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The hepatotoxicity of tributyltin chloride (TBTC) and dibutyltin dichloride (DBTC) was compared among mice, rats and guinea pigs in vivo. Further, the metabolism of these butyltin compounds in the liver was also investigated in these species. The oral administration of TBTC and DBTC to mice induced obvious liver injury, as demonstrated by both serodiagnosis and histopathological diagnosis. The concentrations of TBTC and DBTC that induced hepatotoxicity in mice at 24 h after oral administration were 180 and 60 micro mol/kg, respectively. In the case of rats, the liver injury induced by TBTC and DBTC was detected at 24 h by the serodiagnosis, but not by histopathological diagnosis. On the other hand, in guinea pigs, TBTC and DBTC administration did not produce any clear liver injury at 24 h, as evaluated by these two diagnostic methods. Thus, the following ranking was obtained with regard to increasing order of sensitivity to liver injury caused by TBTC and DBTC: mice, rats and guinea pigs. The total butyltin contents in the liver of mice were equivalent at 3 h and 24 h after the administration of TBTC or DBTC; however, the contents in the liver of rats and guinea pigs were relatively lower at 3 h and higher at 24 h than those of mice, although there were no differences between rats and guinea pigs in the total liver butyltin content. Concerning the liver metabolism of these butyltin compounds, the main form of butyltin compounds in these animals treated with TBTC was DBTC within 3 h after oral administration, while the main metabolites at 24 h were different in each species, indicating that the liver metabolism of TBTC might vary by animal type. When the animals were treated with DBTC orally, DBTC was hardly metabolized in the livers of these animals even at 24 h, and the liver levels of DBTC were two times greater in mice and guinea pigs than in rats at 3 h and were lower in mice at 24 h than in rats and guinea pigs. The analysis of cellular distributions of DBTC in the liver at 3 h after the administration showed that the levels of DBTC in the nuclear, microsomal and mitochondrial fractions of mice hepatocytes were relatively higher than in those of rats, which were greater than in those of guinea pigs. These results suggest differences in the sensitivity of mice, rats and guinea pigs to hepatotoxicity caused by butyltin compounds and demonstrate that the difference in the sensitivity of these animals to the hepatotoxicity induced by TBTC and DBTC may be partly due to differences in hepatic metabolism of TBTC and in the distribution of DBTC within cell organelles, respectively.

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Section: Introductionmentioning

confidence: 96%

Comparison of hepatotoxicity and metabolism of butyltin compounds in the liver of mice, rats and guinea pigs

et al. 2003

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“…Correlation of the alkyllead levels in gull tissue suggest that sequential metabolic dealkylation of the alkylleads, as reported in mammals (40), occurred. Trimethyllead and Me2Pb2+ levels in liver and kidney samples of combined (mature and immature) birds (Table VII) were significantly correlated (p = 0.05, Pearson correlation coefficients).…”

Section: Resultsmentioning

confidence: 80%

Ionic alkylleads in herring gulls from the Great Lakes region

Forsyth¹,

Marshall²

1986

Environ. Sci. Technol.

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“…More importantly, vicinal cysteine residues have been implicated in the progressive dealkylation of organotin compounds in both bacteria and mammals [13,28,47,48], with a mechanism similar to the degradation of alkyllead and alkylmercury compounds [49,50]. In particular, the organotin dealkylation carried out by the dithiols of SNN-PEP shows similarities to the degradation of organomercurials into inorganic Hg(II) by organomercurial lyase (MerB) in bacteria resistant to organomercurial compounds [51][52][53][54].…”

Section: Is the Mechanism Of Dealkylation Of Organotin Compounds Simimentioning

confidence: 96%

Biological chemistry of organotin compounds: Interactions and dealkylation by dithiols

Buck‐Koehntop

Porcelli

Lewin

et al. 2006

Journal of Organometallic Chemistry

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Oxidative Dealkylation of Tetra-, Tri-, and Dialkyltins and Tetra- and Trialkylleads by Liver Microsomes.

Cited by 56 publications

References 0 publications

Comparison of hepatotoxicity and metabolism of butyltin compounds in the liver of mice, rats and guinea pigs

Comparison of hepatotoxicity and metabolism of butyltin compounds in the liver of mice, rats and guinea pigs

Ionic alkylleads in herring gulls from the Great Lakes region

Biological chemistry of organotin compounds: Interactions and dealkylation by dithiols

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