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.

Zinc Toxicity: Does It Exist?:

Abstract: Zinc is an indispensable trace element and is a constituent of more than 200 enzymes. It can assure the stability of biological molecules such as DNA, or biological structures such as membranes or ribosomes. It is not surprising, therefore, that, compared with zinc toxicity, zinc deficiency is a much more frequent risk. Few acute toxic effects have been ascribed to zinc and no long-term effects were found after single or prolonged exposure at doses below 1 g/kg of food. Zinc is neither mutagenic nor carcinogenic, although its levels may influence tumor growth. Zinc appears not to be teratogenic but, on the contrary, deleterious action on zinc deficiency on the developing organisms is well documented.

Effect of sublethal concentration of mercury and zinc on the energetics of a freshwater fish Cyprinus carpio (Linnaeus).

Abstract: Exposure of a freshwater fish Cyprinus carpio to the sublethal concentration of mercury (0.1 mg L-1) and zinc (6.0 mg L-1) resulted in distinct changes in the energy metabolism of gill, liver and muscle at 1, 15 and 30 days. The changes were: (a) The rate of oxygen consumption and SDH activity decreased in the organs of mercury-exposed fish at all the three exposure periods in the order 1 > 15 15 > 30 days. (b) The activity of LDH and the levels of pyruvate and lactate increased in all the three organs of the fish at the three exposure periods studied in both the metal media. But, this increase was also in the order 1 > 15 15 > 30 days in the organs of the fish exposed to mercury and zinc, respectively. (c) The results indicated greater reliance of mercury exposed fish on the energetically less efficient anaerobic glycolysis as the oxidative metabolism suppressed, and the dependency of zinc-exposed fish on both the oxidative and anaerobic glycolytic pathways in order to meet the energy requirements. On prolonged exposure zinc-exposed fish could adapt to sublethal toxic stress, such type of adaptive-response was not observed in mercury-exposed fish.

Zinc at cytotoxic concentrations affects posttranscriptional events of gene expression in cancer cells.

Abstract: Zinc at cytotoxic concentrations has been shown to regulate gene transcription in cancer cells, though zinc's involvement in posttranscriptional regulation is less characterized. In this study, we investigated the involvement of cytotoxic zinc in the posttranscriptional steps of gene expression. Clioquinol, a well-established zinc ionophore, was used to raise intracellular zinc to reported cytotoxic levels. The MCF-7 human cancer cell line was applied as a cell model system. Several parameters were used as indictors of posttranscriptional regulation, including p-body formation, microRNA profiling, expression level of proteins known to regulate mRNA degradation, microRNA processing, and protein translation. p-body formation was observed in MCF-7 cells using several molecules known as p-body components. Clioquinol plus zinc enhanced p-body assembly in MCF-7 cells. This enhancement was zinc-specific and could be blocked by a high affinity zinc chelator. The enhancement does not seem to be due to a stress response, as paclitaxel, a commonly used chemotherapeutic, did not cause enhanced p-body formation at a highly cytotoxic concentration. microRNA profiling indicated that clioquinol plus zinc globally down-regulates microRNA expression in this model system, which is associated with the reduced expression of Dicer, an enzyme key to microRNA maturation, and Ago2, a protein essential for microRNA stability. This study demonstrates that ionophoric zinc can induce cytotoxicity in cancer cells by globally regulating posttranscriptional events.