[“Molecule Logo

Superoxide can be transformed into hydrogen peroxide via superoxide dismutase.ROS is found to have a deleterious eect on lipids by being involved in lipid peroxidation to malondialdehyde, protein carbonyls, and oxidation of guanine into oxodeoxyguanosine in DNA. Cardiolipin is a phospholipid found in the inner mitochondrial membrane and is involved specically with the proteins of the electron transport chain.It is exclusively required by adenine nucleotide translocase, which functions as an inner membrane transporter.The enrichment of cardiolipin in polyunsaturated fatty acids such as linoleic acid and the location adjacent to the sites of ROS production in the mitochondrial electron transport chain make it a primary target for ROS.CL is prone to oxidation, leads to mitochondrial electron transport chain dysfunction, and is supposed to be involved in the release of proapoptotic proteins. ROS has a direct damaging eect on proteins and lipids, which hinder the bioenergetics function in mitochondria.It also causes a deleterious eect on mitochondrial DNA, directly associated with promoter inactivation and downregulation of mitochondrial gene expression.Therefore, it is assumed that elevated levels of ROS production in mitochondria, which have longer halflivessuch as HO; lipid hydroperoxide; or active aldehydes like MDA, acrolein, and so on can cause mitochondrial dysfunction and ultimately hinder biological processes leading to various diseases.The involvement of mitochondria and mitochondrial dysfunction owing to ROS in various diseases is schematically depicted in. The brain is highly enriched in oxidizable substrates. The high oxygen demand, relatively less antioxidant enzymes, and abundance of catalytic transition metal in some regions of the brain make it more vulnerable to oxidative damage. Oxidatively damaged mt DNA leads to various point mutations, which were demonstrated by cloning and sequencing methods. A common deletion evidenced in aged persons, found to be accumulated in mt DNA, is the result of oxidative lesions caused by ROS.The main reason for the highest accumulation of this mutation can be the active involvement of the brain in the oxidative catabolism of dopamine.Various DNA glycosylase present in the cell to repair mt DNA are found to decrease in number with ageing, thus leading to somatic mutations in mt DNA in the aged brain. This awareness increases the inclusion of these ingredients in our daily routine meals.However, the chronic Malic acid health problems and neurodegenerative diseases still occurring raise the possibility that besides antioxidants, there may be other factors associated with oxidative stress, later identied as prooxidants. Thus, prooxidants take in any endobiotic or xenobiotic species, which triggers oxidative stress via producing ROSRNS or inhibits the functioning of the antioxidant system in cells or tissues.Prooxidants may be exogenous and endogenous, which can further be classied in subcategoriesthat is, exogenous is divided into pathogens, drugs, toxicants, dietary ingredients, and so on, and endogenous into anxiety, ion ux, climate, environmental pollution, drug metabolites, and so on.Some antioxidant avonoids are reported to behave as prooxidants in the presence of some transition metals.It is the avonoid structure that majorly contributes to the antioxidant properties as well as copperinitiated Secnidazole prooxidant behavior.In avonoids, OH substitution leads to the antioxidant property of avonoids, while avone and avanone devoid of OH substitution, facilitating the backbone skeleton of avonoids, lack antioxidant properties as well as copper initiated prooxidant properties.

Leave a Reply