Multiple metal resistance in the ciliate protozoan, Vorticella microstoma, isolated from industrial effluents and its potential in bioremediation of toxic wastes.
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Biomedical subjects
Publications and source records attributed to Riaz-ul-Haq.
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Microorganisms present in water samples from various industrial effluents were analysed for their resistance to lead, chromium, and cadmium. The ability of these microorganisms to grow on or metabolize toxic hydrocarbons and pesticides was also checked. Microorganisms in samples from the steel and tanning industries were generally resistant to metal ions but were not capable of metabolizing toxic hydrocarbons. Conversely, microorganisms found in samples of pesticide and from the chemical industry were capable of metabolizing hydrocarbons and pesticides but were not much resistant to metal ions. Microorganisms from effluents of the paint industry and urban wastes were resistant to lead. A correlation between the population of microorganisms and the type of pollution was observed. Indigenous microorganism could be regarded as indicators of pollution and be used in various operations to resist, process, metabolize, and detoxify toxic industrial wastes.
It is generally accepted that Bacillus thuringiensis (B.t.) is specifically toxic to some insects but does not pose any threat to the environment, operators, or consumers. There are several other Bacillus species which can be used as effective bioinsecticides. In this study four different species of Bacillus, i.e., B. coagulans, B. megaterium, B. brevis, and B. sphaericus were isolated from soil samples collected from Kala Shah Kakoo and Kasur areas, in the suburbs of Lahore. Isolated Bacillus species were administered to mosquito larvae to evaluate their biocidal activity. B. coagulans I from Kala Shah Kakoo showed 93% mortality, while B. coagulans III from Kasur showed 70% mortality. Bacterial isolates most toxic to Anopheles larvae showed optimum growth at 37 degrees C and pH 7. These isolates have a great potency to controlling anopheline population.
Nuclear factor kappaB (NFkappaB) plays a pivotal role in early gene responses by promoting messenger RNA (mRNA) synthesis for various cell-adhesion molecules and inducible nitric oxide synthase. In this study, we examined whether increases in glucose concentration enhance NFkappaB expression in nuclear fractions of endothelial cells by using electrophoretic mobility shift assay. Bovine aortic endothelial cells (BAECs) were incubated in media containing 5.5-35 mM glucose. NFkappaB activity was increased as early as 1 h (peak activation at 2-4 h) after incubation with 35 mM glucose compared with 5.5 mM. Similar increases at 2 h of incubation were observed by using 25 but not 15 mM glucose. Glucose-induced NFkappaB activation was blocked by inhibiting nuclear translocation by using a peptide (SN-50) containing the nuclear-localization sequence of NFkappaB p50 linked to a membrane-permeable motif of the sequence for Kaposi fibroblast growth factor. Co-incubation with a selective protein kinase C (PKC) inhibitor, calphostin C, produced a concentration-dependent inhibition of glucose-induced NFkappaB activation. Thus NFkappaB activation is an early event in response to elevations in glucose, which may elicit multiple pathways contributing to the origin of hyperglycemia- or diabetes-induced endothelial cell injury.
Gallium, a metal with clinical antineoplastic activity, is known to inhibit cellular iron uptake and iron-dependent DNA synthesis. Little information exists regarding the efficacy of gallium in combination with other agents. Since alpha-interferon (IFN-alpha) can modulate the action of certain chemotherapeutic drugs, we examined its influence on the growth inhibitory effects of gallium in CCRF-CEM cells. IFN-alpha and gallium as single agents had only minimal to moderate antiproliferative effects. In combination, however, both drugs synergistically inhibited cell growth, causing cell death accompanied by DNA fragmentation. At lower concentrations (120 microM), gallium inhibited cellular iron uptake but did not increase transferrin receptor expression, nor did it block cellular proliferation. The addition of IFN-alpha to this concentration of gallium significantly increased the gallium-induced block of iron uptake, resulting in an increase in transferrin receptors and an inhibition of cell growth. In contrast, IFN-alpha did not enhance the effects of the iron chelator deferoxamine on iron uptake or cell growth. Our studies suggest that gallium and IFN-alpha synergistically inhibit DNA synthesis through a mechanism that includes inhibition of cellular iron uptake and depletion of intracellular iron below the critical level needed to maintain DNA synthesis.
In this study, we examined effects of retinol deficiency and three retinoids, all-trans-retinoic acid, 13-cis-retinoic acid, and etretin, the aromatic derivative of retinoic acid on nuclear retinoic acid receptor isoforms alpha, beta, and gamma mRNA in rat adipose tissue. Retinol deficiency caused an almost 50% decrease in isoform beta mRNA levels of adipose tissue, whereas little change occurred in the abundance of alpha and gamma isoforms transcripts in this tissue. Intragastric administration of all-trans-retinoic acid to retinol-deficient rats increased the adipose tissue retinoic acid receptor isoforms beta and gamma mRNA levels sixfold and twofold, respectively, in 4 h as compared to adipose tissue of retinol-deficient rats that were administered cottonseed oil. In contrast to this, 13-cis-retinoic acid and etretin at equimolar doses were not effective in inducing beta or gamma isoforms mRNA in retinol-deficient rats. These results show that adipose tissue isoform beta responds to retinol deficiency, and all-trans-retinoic acid rapidly induces beta and gamma mRNA isoforms in this tissue. Thus, retinoic acid may regulate expression of specific genes through its interaction with retinoic acid receptors in adipocytes.
Fatty acid-binding protein (FABP) activity was determined in livers and testes of retinol sufficient, retinol deficient, and also in a group of retinol deficient rats, which were refed 100 micrograms of retinyl acetate for four hours. [14C]palmitoyl CoA binding assay was used to estimate the binding activity of FABP. In retinol sufficient and retinol deficient groups, liver FABP bound 431 and 446 pmol [14C]palmitoyl CoA/mg cytosolic protein respectively. In contrast, testicular FABP bound 254 and 139 pmol [14C]palmitoyl CoA/mg cytosolic protein in retinol sufficient and deficient groups. Retinol deficiency caused a tissue specific change in testicular FABP and not in liver FABP. Liver and testicular FABP's remained unchanged after four hour refeeding of retinol to retinol deficient rats.
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Fatty acyl CoA synthetase (FACS) activities were investigated in fetal, neonatal and adult liver and lung. Lung microsomal FACS activity increased near term, declined after birth and reached adult values in 30-day-old rats. Liver microsomal FACS did not show these changes near term. The post-weaning shift from a high fat diet to regular chow diet resulted in decreased liver FACS activity. Lung FACS did not respond to this change in diet. These data demonstrate that long chain FACS is present in the last 4 days of fetal life and probably contributes to the activation of fatty acids utilized as energy substrate or for the synthesis of phospholipids.