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Probiotics are amply studied and applied dietary supplements of greater consumer acceptance. Nevertheless, the emerging evidence on probiotics-mediated potential risks, especially among immunocompromised individuals, necessitates careful and in-depth safety studies. The traditional probiotic safety evaluation methods investigate targeted phenotypic traits, such as virulence factors and antibiotic resistance. However, the rapid innovation in omics technologies has offered an impactful means to ultimately sequence and unknot safety-related genes or their gene products at preliminary levels. Further validating the genome features using an array of phenotypic tests would provide an absolute realization of gene expression dynamics. For safety studies in animal models, the in vivo toxicity evaluation guidelines of chemicals proposed by the Organization for Economic Co-operation and Development (OECD) have been meticulously adopted in probiotic research. Future research should also focus on coupling genome-scale safety analysis and establishing a link to its transcriptome, proteome, or metabolome for a fine selection of safe probiotic strains. Considering the studies published over the years, it can be inferred that the safety of probiotics is strain-host-dose-specific. Taken together, an amalgamation of in silico, in vitro, and in vivo approaches are necessary for a fine scale selection of risk-free probiotic strain for use in human applications. [ABSTRACT FROM AUTHOR]

This article summarizes a recent globally accepted taxonomic reclassification and nomenclature of the genus Lactobacillus. A group of international scientists led by Dr. Jinshui Zheng noticed a greater phenotypic and genotypic heterogeneity among the species previously classified under the genus Lactobacillus. Hence, researchers reevaluated the phylogeny of 261 species of Lactobacillus. Based on phenotypic and genotypic approaches, the genus Lactobacillus was carved into 25 genera, which comprised Lactobacillus, Paralactobacillus and the 23 novel genera. The nomenclature of 23 novel genera was proposed as mentioned here; Schleiferilactobacillus, Amylolactobacillus, Companilactobacillus, Bombilactobacillus, Lapidilactobaci l lus, Holzapfe l i a, Agrilactobacillus, Lacticaseibacillus, Loigolactobacilus, Dellaglioa, Latilactobacillus, Liquorilactobacillus, Ligilactobacillus, Furfurilactobacillus, Lactiplantibacillus, Paucilactobacillus, Lactiplantibacillus, Limosilactobacillus, Fructilactobacillus, Apilactobacillus, Acetilactobacillus, Secundilactobacillus, Lentilactobacillus and Levilactobacillus. In addition, all genera which were previously included in the family Leuconostocaceae were merged under Lactobacillaceae. In this regard, we briefed the scientific rationale and the methods employed for re-classification of the genus Lactobacillus, while also presenting the former and present nomenclature of a few species of dairy and food relevance. [ABSTRACT FROM AUTHOR]

Abstract: The aim of this study was to investigate the chemopreventive effect of probiotic fermented milk and chlorophyllin on aflatoxin B1 (AFB1) induced hepatocellular carcinoma. In vivo trials were conducted on 200 Wistar rats allocated to eight groups. Rats in the positive control group were given intraperitoneal injection of aflatoxin B1 at 450μg/kg body weight twice a week for 6weeks. The rats were sacrificed and dissected at 25th week of the experiment, and comet assay was carried out in hepatic cells to assess the genotoxicity or DNA damage. The tumour incidence was decreased by approximately one-third than AFB1 control group. The expression of c-myc bax, bcl-2, cyclin D1, p53 and rasp-21 genes was also studied. A significant (P<0.05) reduction in DNA damage was observed in probiotic fermented milk with chlorophyllin group as compared to aflatoxin B1 control group. The c-myc, bcl-2, cyclin D1 and rasp-21 level was found to be highest in AFB1 control group as compared to the treatment group. The results advocate the enhanced protective potential of probiotic fermented milk and chlorophyllin against AFB1-induced molecular alterations in hepatic cells during carcinogenesis. [Copyright &y& Elsevier]