Biomedical subjects

Satyendra K Garg

Publications and source records attributed to Satyendra K Garg.

5 recordsLinked to original sources

PubMed2005

Enhanced biodegradation of beta- and delta-hexachlorocyclohexane in the presence of alpha- and gamma-isomers in contaminated soils.

The chlorinated insecticide hexachlorocyclohexane (HCH) has been used extensively in the past, and contaminated sites are present throughout the world. Toward their bioremediation, we isolated a bacterium Pseudomonas aeruginosa ITRC-5 that mediates the degradation of all the four major isomers of HCH under aerobic conditions, both in liquid-culture and contaminated soils. In liquid-culture, the degradation of alpha- and gamma-HCH is rapid and is accompanied with the release of 5.6 micromole chloride ions and 4.1 micromole CO2 micromole(-1) HCH-isomer. The degradation of beta- and delta-isomers is slow, accompanied with the release of 0.9 micromole chloride ions micromole(-1) HCH-isomer, and results in a transient metabolite 2,3,4,5,6-pentachlorocyclohexan-1-ol. The strain ITRC-5 also mediates the degradation of alpha-, beta-, gamma-, and delta-isomers in contaminated soils, where degradation of otherwise persistent beta- and delta-HCH is enhanced severalfold in the presence of alpha- or gamma-HCH. The degradation of soil-applied beta- and delta-HCH under aerobic conditions has not been reported earlier. The isolate ITRC-5 therefore demonstrates potential for the bioremediation of HCH-wastes and contaminated soils.

Aerobiosis↗

PubMed2004

Proteome analysis of mouse macrophages treated with anthrax lethal toxin.

Anthrax toxin produced by Bacillus anthracis is a tripartite toxin comprising of protective antigen (PA), lethal factor (LF) and edema factor (EF). PA is the receptor-binding component, which facilitates the entry of LF or EF into the cytosol. EF is a calmodulin-dependent adenylate cyclase that causes edema whereas LF is a zinc metalloprotease and leads to necrosis of macrophages. It is also important to note that the exact mechanism of LF action is still unclear. With this view in mind, in the present study, we investigated a proteome wide effect of anthrax lethal toxin (LT) on mouse macrophage cells (J774A.1). Proteome analysis of LT-treated and control macrophages revealed 41 differentially expressed protein spots, among which phosphoglycerate kinase I, enolase I, ATP synthase (beta subunit), tubulin beta2, gamma-actin, Hsp70, 14-3-3 zeta protein and tyrosine/tryptophan-3-monooxygenase were found to be down-regulated, while T-complex protein-1, vimentin, ERp29 and GRP78 were found to be up-regulated in the LT-treated macrophages. Analysis of up- and down-regulated proteins revealed that primarily the stress response and energy generation proteins play an important role in the LT-mediated macrophage cell death.

Adenosine Triphosphate↗

PubMed2004

Occurrence of chromium resistant thermotolerant coliforms in tannery effluent.

Twenty six thermotolerant strains resistant to high levels of chromium (50-250 microg/ml) were isolated from treated tannery effluent. They were also found resistant to multiple heavy metals and antibiotics. Majority of them were resistant to copper and bacitracin. Nine strains representing different resistance patterns were selected for plasmid profile and conjugation studies. Agarose gel electrophoresis results revealed that 6 strains harboured a single plasmid, whereas 3 strains exhibited 2 plasmid bands. Among antimicrobials, co-trimazole and bacitracin and among metals, Cu2+, Cd2+, Zn2+ and Ni2+ resistance were transferred most frequently at variable rates. However, chromium resistance was transferred in 6 strains with a frequency ranging 19-49x10(-2). Resistance to Co2+ and Hg2+ did not transfer under environmental conditions. Among the nine strains, three were found predominantly uropathogenic Escherichia coli (UPEC) serotype 04, whereas two strains were untypable. In addition, 4 transconjugants also showed a positive result after serotyping.

Anti-Bacterial Agents↗

PubMed2003

Immunomodulation by lead.

Lead, a potential human carcinogen, is a ubiquitous environmental pollutant in the industrial environment that poses a serious threat to human health. This toxic lead can modulate the immune response of animals as well as humans. In some instances, the immune system appears to be exquisitely sensitive to lead as compared with other toxicological parameters. Both stimulation and suppression of immune response have been demonstrated in lead exposed animals and humans depending on the T helper (Th)1 vs Th2 response. Although the majority of data accumulated to date pertains to the effects of lead in small laboratory rodents, there is little reason to believe that similar quantifiable effects do not occur in domestic and food-producing animals owing to basic functional similarities of the immune system of mammals. In this review, we have discussed the immunomodulatory role of the toxic heavy metal, lead, on cellular and humoral components of the immune system with particular reference to effector cells such as B cells, T cells, natural killer (NK) cells, and soluble mediators such as cytokines, chemokines, and nitric oxide (NO).

Animals↗

PubMed2002

A physiochemical mechanism of hemozoin (beta-hematin) synthesis by malaria parasite.

Malaria parasite homogenate, the lipid extracts, and an unsaturated fatty acid, linoleic acid, which have been shown to promote beta-hematin formation in vitro, were used to investigate the mechanism of hemozoin biosynthesis, a distinct metabolic function of the malaria parasite. In vitro beta-hematin formation promoted by Plasmodium yoelii homogenate, the lipid extracts, and linoleic acid were blocked by ascorbic acid, reduced glutathione, sodium dithionite, beta-mercaptoethanol, dithiothreitol, and superoxide dismutase. Oxidized glutathione did not show any effect. Preoxidized preparations of the lipids extracts or the P. yoelii homogenate failed to catalyze beta-hematin formation. Depletion of oxygen in the reaction mixtures also inhibited the lipid-catalyzed beta-hematin formation. Under the reaction conditions similar to those used for the in vitro beta-hematin formation assay, the antioxidants and reducing agents mentioned above, except the DTT and beta-mercaptoethanol, did not cause degradation of heme. beta-Hematin formation was also inhibited by p-aminophenol, a free radical chain reaction breaker. Hemozoin biosynthesis within the digestive vacuoles of the malaria parasite may be a lipid-catalyzed physiochemical reaction. An oxidative mechanism may be proposed for lipid-mediated beta-hematin formation, which may be mediated by generation of some free radical intermediates of heme.

Aminophenols↗