Reactive oxygen species, heat stress and oxidative-induced mitochondrial damage. A review

Abstract

In recent years there has been enormous interest in researching oxidative stress. Reactive oxygen species (ROS) are derived from the metabolism of oxygen as by-products of cell respiration, and are continuously produced in all aerobic organisms. Oxidative stress occurs as a consequence of an imbalance between ROS production and the available antioxidant defence against them. Nowadays, a variety of diseases and degenerative processes such as cancer, Alzheimer's and autoimmune diseases are mediated by oxidative stress. Heat stress was suggested to be an environmental factor responsible for stimulating ROS production because of similarities in responses observed following heat stress compared with that occurring following exposure to oxidative stress. This manuscript describes the main mitochondrial sources of ROS and the antioxidant defences involved to prevent oxidative damage in all the mitochondrial compartments. It also deals with discussions concerning the cytotoxic effect of heat stress, mitochondrial heat-induced alterations, as well as heat shock protein (HSP) expression as a defence mechanism.

Does air pollution play a role in infertility?: a systematic review

“…(2) Generation of oxidative stress: NO 2 , O 3 or PM (through the heavy metals and PAHs they contain) can generate reactive oxygen species (ROS) [16][17][18]. These cause alterations in DNA, proteins and membrane lipids [19,20]. (3) Modifications of DNA: Through the formation of DNA adducts, leading to modifications in gene expression and/or the appearance of epigenetic mutations or modifications such as an alteration of DNA methylation [21][22][23].…”

Induction of Oxidative Stress by Hyperthermia and Enhancement of Hyperthermia-Induced Apoptosis by Oxidative Stress Modification

“…We hypothesized that PBN could be a sensitizer of HT-induced apoptosis, because HT causes intracellular oxidative stress [5,6]. Treatment of U937 cells with HT (44 C, 10 min) plus PBN increased the levels of nitrite in the culture medium, whereas this treatment decreased the production of O 2 À [20].…”

“…On the other hand, increased levels of ROS may be detrimental and lead to cell damage and cell death. HT is one of the factors responsive for production of ROS in cells [5,6] (Fig. 2.1).…”

“…It is well known that HT induce apoptosis [10]. Heat stress has also been shown to induce oxidative stresses because of the increased production of reactive oxygen spaces (ROS) [5,6], and oxidative stresses play important roles as intracellular mediators of heat-induced cell death [7][8][9][10].…”

Sensing mechanisms and individuality of heat stress in mammalian cells

“…However stresses such as heat, UV radiation and hypoxia are known to impair this balance and reactive oxygen species damage macromolecules such as proteins, lipids and nucleic acids (Belhadj Slimen et al 2014;Akbarian et al 2016;Yang et al 2010). …”