Antioxidants are compounds that inhibit oxidation,a chemical reaction that can produce free radicals. Autoxidation leads to degradation of organic compounds,including living matter. Antioxidants are frequently added to industrial products,such as polymers,fuels,and lubricants,to extend their usable lifetimes. Food are also treated with antioxidants to forestall spoilage,in particular the rancidification of oils and fats. In cells,antioxidants such as glutathione,mycothiol or bacillithiol,and enzyme systems like superoxide dismutase,can prevent damage from oxidative stress.
Superoxide dismutase (SOD,EC 1.15.1.1) is an enzyme that alternately catalyzes the dismutation (or partitioning) of the superoxide (O−
2) radical into ordinary molecular oxygen (O2) and hydrogen peroxide (H
2O
2). Superoxide is produced as a by-product of oxygen metabolism and,if not regulated,causes many types of cell damage. Hydrogen peroxide is also damaging and is degraded by other enzymes such as catalase. Thus,SOD is an important antioxidant defense in nearly all living cells exposed to oxygen. One exception is Lactobacillus plantarum and related lactobacilli,which use a different mechanism to prevent damage from reactive O−
2.
Xanthine oxidase is a form of xanthine oxidoreductase,a type of enzyme that generates reactive oxygen species. These enzymes catalyze the oxidation of hypoxanthine to xanthine and can further catalyze the oxidation of xanthine to uric acid. These enzymes play an important role in the catabolism of purines in some species,including humans.
Oxygen toxicity is a condition resulting from the harmful effects of breathing molecular oxygen at increased partial pressures. Severe cases can result in cell damage and death,with effects most often seen in the central nervous system,lungs,and eyes. Historically,the central nervous system condition was called the Paul Bert effect,and the pulmonary condition the Lorrain Smith effect,after the researchers who pioneered the discoveries and descriptions in the late 19th century. Oxygen toxicity is a concern for underwater divers,those on high concentrations of supplemental oxygen,and those undergoing hyperbaric oxygen therapy.
Genotoxicity is the property of chemical agents that damage the genetic information within a cell causing mutations,which may lead to cancer. While genotoxicity is often confused with mutagenicity,all mutagens are genotoxic,but some genotoxic substances are not mutagenic. The alteration can have direct or indirect effects on the DNA:the induction of mutations,mistimed event activation,and direct DNA damage leading to mutations. The permanent,heritable changes can affect either somatic cells of the organism or germ cells to be passed on to future generations. Cells prevent expression of the genotoxic mutation by either DNA repair or apoptosis;however,the damage may not always be fixed leading to mutagenesis.
In chemistry and biology,reactive oxygen species (ROS) are highly reactive chemicals formed from diatomic oxygen (O2),water,and hydrogen peroxide. Some prominent ROS are hydroperoxide (O2H),superoxide (O2-),hydroxyl radical (OH.),and singlet oxygen. ROS are pervasive because they are readily produced from O2,which is abundant. ROS are important in many ways,both beneficial and otherwise. ROS function as signals,that turn on and off biological functions. They are intermediates in the redox behavior of O2,which is central to fuel cells. ROS are central to the photodegradation of organic pollutants in the atmosphere. Most often however,ROS are discussed in a biological context,ranging from their effects on aging and their role in causing dangerous genetic mutations.
Liver disease,or hepatic disease,is any of many diseases of the liver. If long-lasting it is termed chronic liver disease. Although the diseases differ in detail,liver diseases often have features in common.
A molecular lesion or point lesion is damage to the structure of a biological molecule such as DNA,RNA,or protein. This damage may result in the reduction or absence of normal function,and in rare cases the gain of a new function. Lesions in DNA may consist of breaks or other changes in chemical structure of the helix,ultimately preventing transcription. Meanwhile,lesions in proteins consist of both broken bonds and improper folding of the amino acid chain. While many nucleic acid lesions are general across DNA and RNA,some are specific to one,such as thymine dimers being found exclusively in DNA. Several cellular repair mechanisms exist,ranging from global to specific,in order to prevent lasting damage resulting from lesions.
Respiratory burst is the rapid release of the reactive oxygen species (ROS),superoxide anion and hydrogen peroxide,from different cell types.
NADPH oxidase is a membrane-bound enzyme complex that faces the extracellular space. It can be found in the plasma membrane as well as in the membranes of phagosomes used by neutrophil white blood cells to engulf microorganisms. Human isoforms of the catalytic component of the complex include NOX1,NOX2,NOX3,NOX4,NOX5,DUOX1,and DUOX2.
Oxidative stress reflects an imbalance between the systemic manifestation of reactive oxygen species and a biological system's ability to readily detoxify the reactive intermediates or to repair the resulting damage. Disturbances in the normal redox state of cells can cause toxic effects through the production of peroxides and free radicals that damage all components of the cell,including proteins,lipids,and DNA. Oxidative stress from oxidative metabolism causes base damage,as well as strand breaks in DNA. Base damage is mostly indirect and caused by the reactive oxygen species generated,e.g.,O2− (superoxide radical),OH (hydroxyl radical) and H2O2 (hydrogen peroxide). Further,some reactive oxidative species act as cellular messengers in redox signaling. Thus,oxidative stress can cause disruptions in normal mechanisms of cellular signaling.
Hyperoxia occurs when cells,tissues and organs are exposed to an excess supply of oxygen (O2) or higher than normal partial pressure of oxygen.
Epidemic dropsy is a form of edema of extremities due to poisoning by Argemone mexicana.
Photoprotection is the biochemical process that helps organisms cope with molecular damage caused by sunlight. Plants and other oxygenic phototrophs have developed a suite of photoprotective mechanisms to prevent photoinhibition and oxidative stress caused by excess or fluctuating light conditions. Humans and other animals have also developed photoprotective mechanisms to avoid UV photodamage to the skin,prevent DNA damage,and minimize the downstream effects of oxidative stress.
Pro-oxidants are chemicals that induce oxidative stress,either by generating reactive oxygen species or by inhibiting antioxidant systems. The oxidative stress produced by these chemicals can damage cells and tissues,for example,an overdose of the analgesic paracetamol (acetaminophen) can fatally damage the liver,partly through its production of reactive oxygen species.
Bacterial glutathione transferases are part of a superfamily of enzymes that play a crucial role in cellular detoxification. The primary role of GSTs is to catalyze the conjugation of glutathione (GSH) with the electrophilic centers of a wide variety of molecules. The most commonly known substrates of GSTs are xenobiotic synthetic chemicals. There are also classes of GSTs that utilize glutathione as a cofactor rather than a substrate. Often these GSTs are involved in reduction of reactive oxidative species toxic to the bacterium. Conjugation with glutathione receptors renders toxic substances more soluble,and therefore more readily exocytosed from the cell.
Arsenic biochemistry refers to biochemical processes that can use arsenic or its compounds,such as arsenate. Arsenic is a moderately abundant element in Earth's crust,and although many arsenic compounds are often considered highly toxic to most life,a wide variety of organoarsenic compounds are produced biologically and various organic and inorganic arsenic compounds are metabolized by numerous organisms. This pattern is general for other related elements,including selenium,which can exhibit both beneficial and deleterious effects. Arsenic biochemistry has become topical since many toxic arsenic compounds are found in some aquifers,potentially affecting many millions of people via biochemical processes.
Central University of Gujarat is a public central research university in Gandhinagar,Gujarat offering courses at undergraduate,postgraduate,and doctoral levels.Rama Shanker Dubey is vice-chancellor of Central University of Gujarat.
All living cells produce reactive oxygen species (ROS) as a byproduct of metabolism. ROS are reduced oxygen intermediates that include the superoxide radical (O2−) and the hydroxyl radical (OH•),as well as the non-radical species hydrogen peroxide (H2O2). These ROS are important in the normal functioning of cells,playing a role in signal transduction and the expression of transcription factors. However,when present in excess,ROS can cause damage to proteins,lipids and DNA by reacting with these biomolecules to modify or destroy their intended function. As an example,the occurrence of ROS have been linked to the aging process in humans,as well as several other diseases including Alzheimer's,rheumatoid arthritis,Parkinson's,and some cancers. Their potential for damage also makes reactive oxygen species useful in direct protection from invading pathogens,as a defense response to physical injury,and as a mechanism for stopping the spread of bacteria and viruses by inducing programmed cell death.
Rhododendrol (RD) also called 4-[(3R)-3-hydroxybutyl]phenol (systemic name),is an organic compound with the formula C10H14O2. It is a naturally occurring ingredient present in many plants,such as the Rhododendron. The phenolic compound was first developed in 2010 as a tyrosinase inhibitor for skin-lightening cosmetics. In 2013,after rhododendrol reportedly caused skin depigmentation in consumers using RD-containing skin-brightening cosmetics,the cosmetics were withdrawn from the market. The skin condition,caused by RD,is called RD-induced leukoderma. Rhododendrol exerts melanocyte cytotoxicity via a tyrosinase-dependent mechanism. It has been shown to impair the normal proliferation of melanocytes through reactive oxygen species-dependent activation of GADD45. It is now well established that rhododendrol is a potent tyrosinase inhibitor.
