Summary Bifidobacteria, naturally present in the dominant colonic microbiota, represent up to 25% of the cultivable faecal bacteria in adults and 80% in infants. As probiotic agents, bifidobacteria have been studied for their efficacy in the prevention and treatment of a broad spectrum of animal and/or human gastrointestinal disorders, such as colonic transit disorders, intestinal infections, and colonic adenomas and cancer. The aim of this review is to focus on the gastrointestinal effects of bifidobacteria as probiotic agents in animal models and man. The traditional use of bifidobacteria in fermented dairy products and the GRAS (‘Generally Recognised As Safe’) status of certain strains attest to their safety. Some strains, especially Bifidobacterium animalis strain DN‐173 010 which has long been used in fermented dairy products, show high gastrointestinal survival capacity and exhibit probiotic properties in the colon. Bifidobacteria are able to prevent or alleviate infectious diarrhoea through their effects on the immune system and resistance to colonization by pathogens. There is some experimental evidence that certain bifidobacteria may actually protect the host from carcinogenic activity of intestinal flora. Bifidobacteria may exert protective intestinal actions through various mechanisms, and represent promising advances in the fields of prophylaxis and therapy.

A strain that efficiently degraded methyl tert-butyl ether (MTBE) was obtained by initial selection on the recalcitrant compound tert-butyl alcohol (TBA). This strain, a gram-positive methylotrophic bacterium identified as Mycobacterium austroafricanum IFP 2012, was also able to degrade tert-amyl methyl ether and tert-amyl alcohol. Ethyl tert-butyl ether was weakly degraded. tert-Butyl formate and 2-hydroxy isobutyrate (HIBA), two intermediates in the MTBE catabolism pathway, were detected during growth on MTBE. A positive effect of Co 2؉ during growth of M. austroafricanum IFP 2012 on HIBA was demonstrated. The specific rate of MTBE degradation was 0.6 mmol/h/g (dry weight) of cells, and the biomass yield on MTBE was 0.44 g (dry weight) per g of MTBE. MTBE, TBA, and HIBA degradation activities were induced by MTBE and TBA, and TBA was a good inducer. Involvement of at least one monooxygenase during degradation of MTBE and TBA was shown by (i) the requirement for oxygen, (ii) the production of propylene epoxide from propylene by MTBE-or TBAgrown cells, and (iii) the inhibition of MTBE or TBA degradation and of propylene epoxide production by acetylene. No cytochrome P-450 was detected in MTBE-or TBA-grown cells. Similar protein profiles were obtained after sodium dodecyl sulfate-polyacrylamide gel electrophoresis of crude extracts from MTBE-and TBA-grown cells. Among the polypeptides induced by these substrates, two polypeptides (66 and 27 kDa) exhibited strong similarities with known oxidoreductases.Methyl tert-butyl ether (MTBE) has been incorporated in reformulated gasoline at concentrations up to 15% (vol/vol) to replace lead tetraethyl in order to comply with the octane index and to reduce the polluting emissions in exhaust gases. Other oxygenates, such as ethyl tert-butyl ether (ETBE) and tert-amyl methyl ether (TAME) and their corresponding alcohols, tert-butyl alcohol (TBA) and tert-amyl alcohol (TAA), can play the same role regarding the octane index. MTBE is the dominant fuel oxygenate (38), with a worldwide production capacity of around 25 million tons. Because of its widespread use and the high frequency of underground tank leakage (35), this compound is now the second most commonly detected contaminant in urban groundwater in the United States (23, 42). In Europe, detectable levels of MTBE in rivers have also been reported (1).The persistence of MTBE in the environment can be ascribed, on the one hand, to its physicochemical properties (i.e., its low adsorption on organic matter and its high solubility in water) and, on the other hand, to its molecular structure (it has both an ether bond and high steric hindrance, which makes it recalcitrant to microbial degradation).Early reports based on microcosms having different origins mentioned the recalcitrance of MTBE and TAME (22) MTBE cometabolism was demonstrated by using propanegrown bacteria (35), an n-butane-grown fungus (17), camphorgrown Pseudomonas putida CAM (36), pentane-grown Pseudomonas aeruginosa (14), ETBE-grown Rhodococcus ruber IFP 2007 (...

Effects of insulin and phorbol esters on subcellular distribution of protein kinase C (PKC) isoforms were examined in rat adipocytes. Both agonists provoked rapid decreases in cytosolic, and/or increases in membrane, immunoreactive PKC-alpha, PKC-beta, PKC-gamma, and PKC-epsilon. Effects of phorbol esters on PKC-alpha redistribution to the plasma membrane, however, were much greater than those of insulin. In contrast, insulin, but not phorbol esters, stimulated the translocation of PKC-beta to the plasma membrane, and provoked changes in PKC-zeta redistribution. Neither agonist altered subcellular distribution of PKC-delta, which was detected only in membrane fractions. Our findings indicate that insulin and phorbol esters have overlapping and distinctly different effects on the subcellular redistribution of specific PKC isoforms.