Sie befinden Sich nicht im Netzwerk der Universität Paderborn. Der Zugriff auf elektronische Ressourcen ist gegebenenfalls nur via VPN oder Shibboleth (DFN-AAI) möglich. mehr Informationen...
Heavy metal-induced cellular and organismal toxicity have become a major health concern in biomedical science. Indiscriminate use of heavy metals in different sectors, such as, industrial-, agricultural-, healthcare-, cosmetics-, and domestic-sectors has contaminated environment matrices and poses a severe health concern. Xenobiotics mediated effect is a ubiquitous cellular response. Oxidative stress is one such prime cellular response, which is the result of an imbalance in the redox system. Further, oxidative stress is associated with macromolecular damages and activation of several cell survival and cell death pathways. Epidemiological as well as laboratory data suggest that oxidative stress-induced cellular response following heavy metal exposure is linked with an increased risk of neoplasm, neurological disorders, diabetes, infertility, developmental disorders, renal failure, and cardiovascular disease. During the recent past, a relation among heavy metal exposure, oxidative stress, and signaling pathways have been explored to understand the heavy metal-induced toxicity. Heavy metal-induced oxidative stress and its connection with different signaling pathways are complicated; therefore, the systemic summary is essential. Herein, an effort has been made to decipher the interplay among heavy metals/metalloids (Arsenic, Chromium, Cadmium, and Lead) exposures, oxidative stress, and signal transduction, which are essential to mount the cellular and organismal response. The signaling pathways involved in this interplay include NF-κB, NRF2, JAK-STAT, JNK, FOXO, and HIF.
•Redox homeostasis is a key to healthy/normal cellular function.•Chromium, cadmium arsenic, and lead toxicity are mediated by oxidative stress.•Heavy metal-ROS-signal transduction leads to the risk of developing diseases.•NF-κB, NRF2, JAK-STAT, JNK and FOXO are the key partner of heavy metal-induced ROS.