Purpose: To investigate the probable antioxidant, antimicrobial and antipancreatic lipase effects of fermented Camellia japonica leaf extracts. Methods: Camellia japonica leaves fermented with Nuruk were extracted using methanol and ethanol. Total phenolic, flavonoid, carotenoid and L-ascorbic acid contents were determined by UV-visible spectrophotometry. The antioxidant activities of these extracts were determined by free radical scavenging, ferrous ion chelating and reducing power assays. Their antimicrobial properties against Gram-positive Staphylococcus epidermidis and Bacillus subtilis, and Gram-negative Klebsiella pneumonia and Escherichia coli bacteria were evaluated by disc diffusion method. Inhibition of pancreatic lipase was measured based on the hydrolytic reaction of p-nitrophenyl butyrate with pancreatic lipase. Results: The ethanol extracts of fermented Camellia japonica leaves exhibited higher phenolic (32274 mg GAE/100 g) and flavonoid (20519 mg RE/100 g) contents with higher superoxide (IC50 = 0.23 mg/mL), hydrogen peroxide (IC50 = 0.28 mg/mL) radical scavenging and ferrous ion chelating (IC50 = 0.21 mg/mL) activities than those of methanol. These ethanol extracts also showed higher antimicrobial activities against all bacterial strains tested with higher inhibitory effects on pancreatic lipase than methanol extracts. Conclusion: The results highlight the possible use of fermented Camellia japonica leaf extracts as a source of antioxidant, antibacterial and antiobesity agents. Ethanol is recommended as solvent for extracting antioxidants, antibacterial and antiobesity agents from this plant.
Potential toxicological interactions of 4-(N-methyl-Nnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) and/or dibuthyl phthalate (DBP) on ozone were investigated after 32-and 52-wk exposures using hprt mutation assay. Male and female B6C3F1 mice exposed to ozone (0.5 ppm), NNK (1.0 mg/kg), DBP (5,000 ppm), and two or three combinations of these toxicants 6 h per day for 32-and 52-wk showed increases in the frequencies of TG r lymphocytes compared to the control groups. Additive interactions were noted from two combination groups compared to the ozone alone in both sexes of 32-and 52-wk studies. The most common specific mutation type in the hprt genes of test materials-treated male and female mice was transversion with very few transition. The results indicate that such dominant transversion may be responsible for toxicity and combined exposure to ozone, NNK, and DBP induces additive genotoxicities compared to ozone alone.
Objective: The purpose of the current work was to characterize mechanisms of cytotoxicity and mutagenesis of a potential human bladder carcinogen 2,6-dimethylaniline (2,6-DMA).Methods: Chinese hamster ovary (CHO) AS52 cells were exposed to either human S9 activated 2,6-DMA for 6 h or its N-hydroxylamine and aminophenol metabolites for 1 h in serum-free medium. Cell survival determined by trypan blue exclusion 24 h after treatment, and 6-thioguanineresistant mutants at the xanthine-guanine phosphoribosyltransferase (gpt) gene locus were assessed with doses of which relative survival is 30% or more. Nested PCR-based deletion analysis was also performed.Results: AS52 cells exhibited a dose-dependent increase in cytotoxicity and mutant fraction upon treatment of 2,6-DMA and its metabolites, but showing considerable variation in potency with aminophenol metabolites having the highest potency and parent compound at least; at the highest 2,6-dimethyaminophenol dose (10 μM), the mutant fraction in AS52 cells was 8 fold (13.2×10 -5 ) greater than the spontaneous fraction of 1.62×10 -5
Conclusion:These findings indicate the mutagenicity of 2,6-DMA at the gpt gene, which is mediated through hydroxylamine and aminophenol metabolites, and contribute to the elucidation of mechanisms through which 2,6-DMA may exert its effects in vivo.. Total deletion of the gpt gene sequences was found in 1 (4%) of spontaneous and 2 (6%) of the 6-thioguanine mutants generated by N-hydroxy-2,6-DMA.
Purpose: To examine the role of endogenous nitric oxide (NO • ) and influence of p53 status during apoptosis induced by a selective iNOS inhibitor, N- [(3-aminomethyl)
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