Synergistic antimicrobial activity of tea & antibiotics.

Tea leaves are known for its antibacterial activity against many microorganisms. In this study we attempted to describe the synergistic antimicrobial activity of tea and antibiotics against enteropathogens. Antimicrobial activity of boiled water tea extract and organic solvent extract were studied against Salmonella typhimurium 1402/84, S. typhi, S. typhi Ty2a, Shigella dysenteriae, Yersinia enterocolitica C770, and Escherichia coli (EPEC P2 1265) determining minimum inhibitory concentration (MIC), minimum bactericidal concentration (MBC) and death rate kinetics at MBC of tea extract in presence of subinhibitory concentration of antibiotic. Both green tea or black tea extracts effectively inhibited the growth of S. typhimurium 1402/84, S. typhi, S. typhi Ty2a, S. dysenteriae, Y. enterocolitica C770, and E.coli (EPEC P2 1265). However, the growth inhibitory concentration of tea extract was lower for green tea as compared to black tea extract. Antimicrobial activity of green tea tea methanol: water extract tea was better as compared to boiled water tea extract of green tea. Based on death rate kinetics results, S.typhi Ty2a appeared to be highly sensitive and Y. enterocolitica C770 the most resistant. Chloramphenicol and tea extract in combination inhibited the growth of S.dysenteriae at 2.5 microg/ml chloramphenicol (MIC 5 microg/ml) and 5.094 mg/ml black tea extract (MIC 9.089 mg/ml). Tea extract showed synergistic activity with chloramphenicol and other antibiotics like gentamycin, methicillin and nalidixic acid against test strains.

Tobacco habits and risk of lung, oropharyngeal and oral cavity cancer: a population-based case-control study in Bhopal, India.

BACKGROUND: Tobacco habits in India are unique and vary in different regions. Few studies, and none from central India, have reported on type of tobacco used and risk of the most common cancer types in India. We conducted a population-based case-control study to evaluate the risk of tobacco particularly bidi smoking and tobacco quid chewing on the most common cancer sites among males in Bhopal. METHODS: In all, 163 lung, 247 oropharyngeal and 148 oral cavity cancer cases from the Population-Based Cancer Registry records and 260 controls randomly selected from a tobacco survey conducted in the Bhopal population formed the study population. RESULTS: A significant risk of bidi and cigarette smoking with a dose-response relationship was observed for lung and oropharyngeal cancer. Tobacco quid chewing showed no risk for lung, marginally increased risk for oropharyngeal and about a sixfold increased risk for oral cavity cancer. Population-attributable risk per cent (PARP) was observed to be 82.7% and 71.6% for smokers for the development of lung and oropharyngeal cancer, while the same was found to be 66.1% for tobacco chewers for the development of oral cavity cancer. CONCLUSIONS: These data provide strong evidence that smoking bidi is even more hazardous than cigarette smoking in the development of lung and oropharyngeal cancer. An intervention study to prevent the use of tobacco will be useful in this population as it also underwent gas exposure due to a chemical accident in 1984.

Cancer patterns of lung, oropharynx and oral cavity cancer in relation to gas exposure at Bhopal.

BACKGROUND: In Bhopal, India, on 2 December 1984, a chemical disaster caused by a gas leak mostly of methyl isocyanate (MIC) from the Union Carbide Factory led to massive mortality and morbidity of the population. This is the first study to shed light on the cancer experience of the Bhopal population as a result of exposure to a mixture of gases which have highly toxic and potentially carcinogenic properties. To observe the effect of gas exposure, incidence rates of the three most common cancer sites (lung, oropharynx and oral cavity) from 1987 to 1992 among the municipal wards were studied in males. METHODS: Relative risks (RR) using cases from the cancer registry and controls from a tobacco survey were estimated for the gas-affected regions. RESULTS: Based on a descriptive study the relative risks of 1.4, 1.3 and 0.7 for lung, oropharynx and oral cavity cancer, respectively, for gas-affected regions in the year 1992 in comparison to gas-unaffected regions and the year 1987-1990 combined were estimated. In the case-control study the RRs of 0.9, 1.4 and 1.2 for lung, oropharynx (adjusted for smoking) and oral cavity cancer, respectively, (adjusted for tobacco chewing) were estimated as the effect of the gas accident. CONCLUSION: The full potential of excess risk, if any, may not manifest for 15-20 years after the accident.

The bacterial hemoglobin from Vitreoscilla can support the aerobic growth of Escherichia coli lacking terminal oxidases.

Two Escherichia coli mutants that lack both cytochrome o and d terminal oxidases are able to grow with glucose as the carbon source but not with the aerobic substrates succinate or lactate. One of these, GV101, is a deletion mutant of cytochrome o and a point mutation of cytochrome d. The other, GK100, is a total deletion mutant of all the genes for both cytochromes. When these mutants were transformed with a plasmid containing the gene for the bacterial hemoglobin from Vitreoscilla, they were capable of growth in the presence of succinate or lactate and showed aerobic respiration in the presence of these substrates, unlike the parent strains. Cells transformed with a plasmid containing the gene for the hemoglobin but lacking the native promoter did not express the hemoglobin and did not respire. Membrane vesicles prepared from the cells consumed oxygen in the presence of succinate. This succinate-supported respiration decreased with successive washings of the vesicles but was restored by adding E. coli cytosol containing the hemoglobin or by adding the hemoglobin purified from Vitreoscilla. This respiration was inhibited by cyanide.

Study of Vitreoscilla globin (vgb) gene expression and promoter activity in E. coli through transcriptional fusion.

Bacterial hemoglobin (VtHb) is produced by the gram-negative bacterium, Vitreoscilla, in large quantity in response to hypoxic environmental conditions. The vgb gene coding for VtHb has been cloned in E. coli where it is expressed strongly by its natural promoter. The expression of the vgb gene in Vitreoscilla is transcriptionally regulated by oxygen. When E. coli cells were shifted from 20% to 5% oxygen, vgb specific transcript increased. In E. coli cells with plasmids carrying transcriptional fusions of the vgb gene promoter to either CAT (chloramphenicol acetyl transferase) or xylE (catechol-2,3-dioxygenase) genes, the promoter activity depended on the oxygen level. The concentration of CAT and xylE gene products in cells grown under 5% oxygen was 5-7 times that of aerobically (20% oxygen) grown cells. When the vgb gene promoter was deleted, VtHb was not produced under any conditions. When the promoter was replaced by the E. coli tac promoter, hypoxic oxygen did not affect the level of expression of vgb, but adding IPTG did increase the expression of this gene. These results indicate that the vgb gene promoter is transcriptionally regulated by oxygen even in E. coli, and that microaerobiosis is sufficient to induce vgb expression. The size of S1 nuclease-resistant hybrids, prepared using RNA transcripts protected with restriction enzyme fragments containing the promoter proximal region of vgb, was the same for both Vitreoscilla and E. coli, further evidence that the same promoter is used in both organisms. Transcriptional fusion of the vgb gene promoter to the xylE reporter gene on the broad host range plasmid, pKD-49, was used to demonstrate that the vgb promoter can be expressed in other gram-negative organisms, including Pseudomonas, Azotobacter, and Rhizobium.