Zinc toxicity

About: Zinc toxicity is a research topic. Over the lifetime, 727 publications have been published within this topic receiving 34583 citations. The topic is also known as: zinc poisoning.

A Novel Zinc Exporter CtpG Enhances Resistance to Zinc Toxicity and Survival in Mycobacterium bovis

Abstract: Tuberculosis is caused by the bacillus Mycobacterium tuberculosis and is one of the major sources of mortality. M. tuberculosis has developed unique mechanisms to adapt to host environments, including zinc deficiency and toxicity, during infection. However, the molecular mechanism by which mycobacteria promote detoxification of zinc, and the associated signaling pathways remains largely unclear. ABSTRACT Zinc is a microelement essential for the growth of almost all organisms, but it is toxic at high concentrations and represents an antimicrobial strategy for macrophages. Mycobacterium tuberculosis and Mycobacterium bovis are two well-known intracellular pathogens with strong environmental adaptability, including zinc toxicity. However, the signaling pathway and molecular mechanisms on sensing and resistance to zinc toxicity remains unclear in mycobacteria. Here, we first report that P1B-type ATPase CtpG acts as a zinc efflux transporter and characterize a novel CmtR-CtpG-Zn2+ regulatory pathway that enhances mycobacterial resistance to zinc toxicity. We found that zinc upregulates ctpG expression via transcription factor CmtR and stimulates the ATPase activity of CtpG. The APC residues in TM6 is essential for CtpG to export zinc and enhance M. bovis BCG resistance to zinc toxicity. During infection, CtpG inhibits zinc accumulation in the mycobacteria, and aids bacterial survival in THP-1 macrophage and mice with elevated inflammatory responses. Our findings revealed the existence of a novel regulatory pathway on mycobacteria responding to and adapting to host-mediated zinc toxicity. IMPORTANCE Tuberculosis is caused by the bacillus Mycobacterium tuberculosis and is one of the major sources of mortality. M. tuberculosis has developed unique mechanisms to adapt to host environments, including zinc deficiency and toxicity, during infection. However, the molecular mechanism by which mycobacteria promote detoxification of zinc, and the associated signaling pathways remains largely unclear. In this study, we first report that P1B-type ATPase CtpG acts as a zinc efflux transporter and characterize a novel CmtR-CtpG-Zn2+ regulatory pathway that enhances mycobacterial resistance to zinc toxicity in M. bovis. Our findings reveal the existence of a novel excess zinc-triggered signaling circuit, provide new insights into mycobacterial adaptation to the host environment during infection, and might be useful targets for the treatment of tuberculosis.

Zinc and docosahexaenoic acid metabolism in brain cells

Abstract: This thesis examines the direct interaction of Docosahexaenoic acid (DHA, an omega-3 fatty acid) against zinc-induced mitochondrial dysfunction and involvement of bioenergetic regulation as a zinc toxicity target, which may be the initiator of oxidative stress, caspase cascade, alteration in epigenetic patterns and therefore gene expression in human neuronal cells.

The effect of heavy metal salts on the embryonic development of the common frog

Abstract: To elaborate methods of biological testing during monitoring of the environment, a study was made of the effect of heavy metal salts on frog embryos and of the influence of temperature on the extent of toxicity of these substances. It was shown that the early stages of embryogenesis were more sensitive to this toxic effect. The differences in the effect of heavy metals are expressed not only in the extent of toxicity, but also in the pattern of change in toxicity as related to concentration. A rise in temperature of the solution containing heavy metals results in a relative increase in the number of abnormal larvae, whereas a decrease in temperature of the solution leads to a higher mortality at the earliest stages of embryogenesis. The latter, apparently, is due to a longer duration of development at low temperature, and thus, to a longer exposure of embryos to toxic effect. This is more pronounced at earlier stages of development, more vulnerable (sensitive) to toxicants. The estimation of toxicity of a substance by the pathological changes induced in embryos and larvae is one of the most sensitive methods, which allows not only to determine the extent of toxicity, but also to give prognosis of its possible effect on the population.

Effect of zinc toxicity on the blood parameters of the laboratory mice

Abstract: The present search conducted at thecollegeofVeterinary Medicine–Universityof Basrahto investigate the effect of zinc toxicity on the physiological parameters, histopathological changes and reproductive efficiency in the laboratory mice. In this search, 32 mice were used, they were divided into two groups, each one consisted of four equal subgroups with 4 mice in each. The first three subgroups of each group were dosed via intraperitoneal injection with 60, 80 and 100 mg/kg zinc in the form of ZnSO 4 for 15 and 30 days. An equivalent volume of saline (0.9 %N.S) was administered to the fourth subgroup which was set as the control group. The investigation of blood parameters included RBC count, Hb concentration, PCV concentration, total and differential WBC count. The results here showed a significant decrease (P≤0.05) of RBC count, Hb concentration, PCV value, and neutrophil count, whereas there was a significant increase (P≤0.05) of total WBC count, lymphocyte count, monocyte count, and there were no significant differences in the acidophil count and basophil count.