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PubMed1979

Prevention of the mutagenic activation of an antischistosomal isothiocyanate in primates by an antibiotic.

Administration of 4 nitro-4' isothiocyano-diphenylamine (CGP 4540, amoscanate) to two nonhuman primates, Macaca mulatta and Cebus apella, resulted in the appearance of mutagenic material in the urines of these animals. Mutagenic metabolites of this drug could also be detected in the urines when the drug was administered to primates infected with Schistosoma mansoni and Schistosoma japonicum. As observed previously in mice, the mutagenic activation of amoscanate can be prevented in primates by coadministration of a single oral dose of erythromycin with no concomitant reduction in antischistosomal activity. The protective effect of erythromycin was confirmed in several crossover experiments. This dissociation of mutagenic from chemotherapeutic effects provides an opportunity to reduce serious potential long-term risks of this antischistosomal drug.

Aniline Compounds↗
PubMedDate not supplied

Protection by antibiotics against experimental focal cholangitis produced in mice by a schistosomicidal isothiocyanate.

Oral administration to mice of high doses of 4-isothiocyano-4'nitrodiphenylamine (amoscanate), a potent antischistosomal drug, produced focal necrotizing lesions of the large intrahepatic and extrahepatic bile ducts and the gallbladder. Coadministration of erythromycin and, to a somewhat lesser degree, of paromomycin, markedly reduced the effects of amoscanate on the biliary tract. These results suggest that amoscanate may be converted to a cholangiotoxic product by one or several constituents of the enteric bacterial flora. Since erythromycin does not affect the antischistosomal activity of amoscanate, coadministration of an antibacterial agent can reduce toxic effects of a drug while full chemotherapeutic activity is maintained. The possibility of toxic effects of metabolites of xenobiotics produced by intestinal bacteria deserves attention and the experimental production of focal intrahepatic and extrahepatic cholangitis by such drug metabolites suggests a possible mechanism in human bile diseases.

1-Naphthylisothiocyanate↗
PubMed2007

Selective cytotoxicity of benzyl isothiocyanate in the proliferating fibroblastoid cells.

In the present study, experiments using presynchronization culture cells demonstrated that benzyl ITC (BITC), previously isolated from a tropical papaya fruit extract, induced the cytotoxic effect preferentially in the proliferating human colon CCD-18Co cells to the quiescent ones. Quiescent CCD-18Co cells were virtually unaffected by BITC and marginal cytotoxicity was observed at 15 microM. We observed that BITC dramatically induced the p53 phosphorylation and stabilization only in the quiescent (G(0)/G(1) phase-arrested) cells, but not significantly in the proliferating human colon CCD-18Co cells when compared with quiescent ones. We also observed ataxia telangiectasia-mutated (ATM) phosphorylation in the quiescent cells. The BITC-induced p53 phosphorylation was counteracted by caffeine treatment, implying the involvement of an ATM/ataxia telangiectasia and Rad3-related kinase signaling pathway. Moreover, downregulation of p53 by a siRNA resulted in the enhancement of susceptibility to undergo apoptosis by BITC. We also showed here that depletion of p53 abrogated G(0)/G(1) arrest accompanied by the declined expression of p21(waf1/cip1) and p27(kip1) in CCD-18Co cells. In conclusion, we identified p53 as a potential negative regulator of the apoptosis induction by BITC in the normal colon CCD-18Co cells through the inhibition of cell-cycle progression at the G(0)/G(1) phase.

Apoptosis↗