Ascorbic acid may also have a toxic eect owing to its autooxidation, leading to inuence gene expression. Heavy metals in combination with other xenobiotics like pesticides exert a deteriorating eect on hematology and the immune system.It has been extensively studied that exposure of elevated levels of heavy metals such as lead, lead to oxidative stress.This leads to the abnormality in redox status of the cell, resulting in a cysteine deleterious eect on biomolecules, as well as vital organs such as the liver, kidney, and CNS. Oxidative stress induced by mercury causes membrane damage and oxidation of biomolecules, and also promotes synthesis of HO, lipid peroxidation in the mitochondrial membrane, and protein oxidation. Mercury is also found to be neurotoxic and prolonged exposure to mercury causes a deleterious eect on the brain, resulting in timidity, tremors, memory problems, and changes in hearing and vision. Lead, a metal used abundantly worldwide, is found to be toxic to humans specically because of induction of oxidative stress.The damage due to lead depends on the route of exposure, health status, its dose, amount of exposure, as well as age of the subject and metal cofactors, which results in a reduction of the activity of antioxidant enzymes involved in various biological processes.It is also associated with elevation in oxidative stress and mitochondrial dysfunction, leading to the failure of vital organs. In addition, arsenic is a metalloid also found to be toxic for living organisms, as the prolonged exposure to arsenic leads to carcinogenesis, cytotoxicity, and Honokiol genotoxicity in humans.Arsenic is also prone to bind with the SH group of glutathione, which leads to the modication of GSH to GSSG, owing to which HO is produced. Arsenic is involved in the inhibition of glucose absorption in cells, causing gluconeogenesis and fatty acids oxidation.The oxidative stress induced ferroptosis and mitochondrial dysfunctiondysregulation, resulting in neuronal cell death as well as cell apoptosis, has been recently demonstrated in PC cells.This study might be extended to solve and throw light on oxidative stress based strategies for protective measures in ND. Cellular apoptosis, also known as programmed cell death, is a natural phenomenon, which occurs as a spontaneously regulated process in a biological system. Along with normal ageing, ROS is also one of the major factors in cellular senescence that leads to the increase in the number of senescent cells in tissues on a large scale.As discussed in previous sections, biomolecules act as biomarkers of oxidative stressthey help in the identication of OS assisted cellular senescence and apoptosis. Elevated level of ROS along with a decrease in antioxidants can cause various agerelated pathologies and diseases such as cancer, cardiovascular, and neurodegenerative diseases.Exposure to elevated levels of ROS disturbs cellular homeostasis, leading to harmful eects on biomolecules.Cellular senescence can happen to multiple cell types including epithelial cells, lymphocytes, chondrocytes, neurons, and glial cells. OS and mt ROS trigger telomere shortening and dysfunction, and in turn cause cellular senescence.ROS cause a deleterious eect on neuronal cells and thus can have harmful eects on brain.ROS mediated cell signaling is an eective indicator of cell apoptosis.