Salmonella typhimurium inhibition

The results on the cellular protection against N()2 can be interpreted as the N()2 reacting with the three antioxidants to produce their radicals, with ascorbic acid reacting least efficiently, probably due to the lower reduction potential of its radical. Moreover, Arroyo et al. (1992) reported that NO - and N02 -induced mutations in Salmonella typhimurium TA1535 were inhibited efficiently by P-CAR and tocopherols, but not at all by ascorbic acid. 

In bacteria and yeasts, Li+ has strain-dependent, inhibitory, and morphological effects upon growth. The driving force behind the transport of carbohydrates and amino acids in bacteria is the proton gradient, and in both E. coli [228] and Salmonella typhimurium cells [229], Li+ stimulates the movement of proline into cells via a Li+/proline symport and the transport of melibiose via a cotransport pathway [230]. In both cases, Li+ is replacing Na+ and results in the inhibition of growth. 

Bessler, H. C., de Oliveira, I. R., and Giugliano, L. G. (2006). Human milk glycoproteins inhibit the adherence of Salmonella typhimurium to HeLa cells. Microbiol. Immunol. 50, 877-882. Bhutta, Z. A., and Yusuf, K. (1997). Early-onset neonatal sepsis in Pakistan A case control study of risk factors in a birth cohort. Am. ]. Perinatol. 14, 577-581. 

Genotoxic Effects. Genotoxic Effects. HDI was demonstrated to be non-mutagenic against some Salmonella typhimurium strains with or without metabolic activation (Anderson et al. 1980). HDI also inhibited the growth of Ehrlich ascites tumor eells in female mice (Moos et al. 1971) and decreased the mutation frequency in Escherichia coli (Kawazoe et al. 1981). Calf thymus DNA incubated in vitro with 10.4 or 52 mol of HDI for 10 or 20 minutes produeed no evidence of intrastrand cross-links or DNA strand breaks (Peel et al. 1997). No studies were located that studied the genotoxic effects of HDI on human cells or that deseribed the ability of prepolymer forms of HDI to induce genotoxicity."... 

Dichloropropene was mutagenic in Salmonella typhimurium, with or without metabolic activation. In one study, the czx-isomer was reported not to be mutagenic to Salmonella typhimurium TAIOO without metabolic activation, and to become active only after exposure to oxygen and consequent generation of autooxidation products. Glutathione was shown to efficiently inhibit the mutagenicity in Salmonella of cis- and trans-... 

Genotoxicity studies with A-hydroxyacetamide, a possible metabolite of acetamide, have shown that this agent is weakly mutagenic in Salmonella typhimurium and induces DNA damage in a rat hepatoma cell line. However, it did not bind covalently to DNA in vitro and did not induce morphological transformation of Syrian hamster embryo cells in vitro or inhibit gap-junctional intercellular communication in Chinese hamster lung V79 cells. 

Activation of allyl chloride to genotoxic substances appears to involve aldehydes, since inhibition of aldehyde dehydrogenase by cyanamide increases the mutagenic activity in Salmonella typhimurium TAIOO on the other hand neither SKF525 nor 1,1,1-tri-chloropropene-2,3-oxide affect the mutagenicity, so that metabolic activation via an epoxide is unlikely (Neudecker Henschler, 1986). 

Antony, U., Moses, L. G., and Chandra, T. S. (1998). Inhibition of Salmonella typhimurium and Escherichia coli by fermented flour of finger millet (Eleusine coracana). World ]. Microbiol. Biotechnol. 14, 883-886. 

Mutagenesis induced in Salmonella typhimurium by 2-fluorenamine and other chemical carcinogens was inhibited by low levels of retinol and other retinoids when carcinogen activation was carried out by rat liver microsomes. In contrast, low levels of retinoids enhanced mutagenesis when carcinogen activation was mediated by whole liver homogenates. There was no effect of the provitamin 3-carotene in this test system. 

Low levels of retinol or retinyl acetate enhance mutagenicity induced by 2-fluorenamine in Salmonella typhimurium when activation is carried out by S9, while inhibiting mutagenicity when activation is mediated by microsomes. 

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