Abstract

Paraquat (PQ) is a non-selective herbicide with strong toxicity to humans and mammals. However, the proteome regulation of cells by PQ is still unclear, limiting the development of effective antidotes. Studies have shown that a slight excess of intracellular copper levels could be beneficial to the survival under exposure to PQ. In this study, Saccharomyces cerevisiae was used as a model to explore the regulation effect of copper ions on PQ poisoning by the approach of date independent acquisition proteomics. The results showed that toxic effect of PQ was primarily induced by oxidative damage in the mitochondria and the disorder of gene expression. The addition of Cu2+ involved a series of favorable reactions to cell survival under PQ stress, including activation of the mitogen-activated protein kinase signaling pathway, regulation of processes such as sulfur metabolism, carbon metabolism and gene expression in cells. The generation of glutathione, heme and steroids advantageous to cell growth under stress was also increased. These findings inferred that therapeutic concentration of copper ions could prolong the survival of cells under PQ stress.

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