Toxic effects of some “mono-n-butyl-tin compounds” on white mice

Pelikán, Z; Cerný, E

doi:10.1007/bf00312376

Cited by 19 publications

(7 citation statements)

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“…Some monobutyltin compounds were shown to cause steatosis of hepatocytes and enlargement of the liver when given to mice as a single oral dose of 4 g/kg body weight (Pelikan and Cerny, 1970). Dibutyltin compounds were considerably more toxic to rodents and caused a specific lesion in bile ducts of rats and mice after a single oral dose of 50 mg/kg or more (Barnes and Magee, 1958).…”

Section: Hepatotoxicitymentioning

confidence: 99%

Biological activity of organotin compounds—An overview

Snoeij

Penninks

Seinen

1987

Environmental Research

346

131

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As a consequence of the rapid expansion of the uses and applications of the organotin compounds, the concern about their environmental and health effects is increasing. The main subject of this overview is the current understanding of the mammalian toxicity of the organotin compounds. Four different types of target organ toxicity, namely neurotoxicity, hepatotoxicity, immunotoxicity, and cutaneous toxicity, are discussed in more detail. The effects of the organotin compounds on the mitochondfial and cellular level are summarized and discussed in relation to the mode of action of these compounds on the central nervous system, the liver and bile duct, the immune system, and the skin. © 1987 Academic Press, Inc. ORGANOTIN COMPOUNDS: APPLICATIONS AND TOXICITY Organotin CompoundsTin can be present as an element in a wide variety of both inorganic and organometallic compounds. Organometallic tin compounds or organotins are characterized by the presence of at least one covalent carbon-tin bond. Although tin may exist either in the Sn 2+ or in the Sn 4+ oxidation state, almost all organotins have a tetravalent structure. Depending on the number of organic moieties, the organotin compounds are classified as mono-, di-, tri-, and tetraorganotins. In compounds of industrial importance, methyl, butyl, octyl, and phenyl groups form the organic substituents, while the anion is usually chloride, fluoride, oxide, hydroxide, carboxylate, or thiolate. All alkyltin compounds refered to in this article contain unbranched saturated hydrocarbon side chains (n-alkyltins).

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Section: Hepatotoxicitymentioning

confidence: 99%

Biological activity of organotin compounds—An overview

Snoeij

Penninks

Seinen

1987

Environmental Research

346

131

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“…In general, the toxicity of organotin compounds is believed to decrease from tri-to mono-organotins and to be dependent upon the number of carbon atoms per side chain (Snoeiji et al 1987;Boyer 1989). For instance, in experimental animals, tributyltin chloride (TBTC) and dibutyltin dichloride (DBTC) have been shown to induce the inflammation of the bile duct associated with hepatic lesions (Barnes and Stoner 1958;Krajnc et al 1984), and acute intestinal pancreatitis (Merkord and Hennighausen 1989), while monobutyltin trichloride (MBTC) is reported to be relatively inert (Pellikan and Cerny 1970). We have also reported that TBTC and DBTC could cause hepatotoxicity, as evaluated by serological criteria, after oral administration to mice, whereas MBTC did not induce liver injury (Ueno et al 1994).…”

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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“…The mechanism by which the liver is damaged by organotin compounds is still unknown, although some authors [12,13] have postulated an impairment of the hepatic transport mechanism or the conjugation of bilirubin with glutathione or both. However, this explanation is not sup ported by our study, because serum bilirubin in these patients remained normal.…”

Section: Casementioning

confidence: 99%

Acute Nephropathy of Organotin Compounds

Lin

Hsueh²

1993

Am J Nephrol

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Three patients who developed acute nephropathy following ingestion of triphenyltin acetate (TPTA) are described. All of them had significant proteinuria, azotemia, and polyuria. Mild neurological manifestations in all patients were also noted. Hematuria and pyuria were noted in 1 severely poisoned patient. Evidence for hepatitis was present in 2 patients, and for pancreatitis in 1. Renal biopsy showed focal fusion of glomerular cell processes and proximal tubular damage with cellular necrosis. Two patients survived with complete recovery of renal functions. One old patient died of aspiration pneumonia. Acute nephropathy following organotin intoxication appears to result mainly from proximal renal tubular damage with a benign and reversible clinical course.

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Toxic effects of some “mono-n-butyl-tin compounds” on white mice

Cited by 19 publications

References 0 publications

Biological activity of organotin compounds—An overview

Biological activity of organotin compounds—An overview

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

Acute Nephropathy of Organotin Compounds

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