Reactive oxygen species and peroxisomes: Struggling for balance

Abstract

Reactive oxygen species (ROS) can surely be considered as multifunctional biofactors within the cell. They are known to participate in regular cell functions, for example, as signal mediators, but overproduction under oxidative stress conditions leads to deleterious cellular effects, cell death and diverse pathological conditions. Peroxisomal function has long been linked to oxygen metabolism due to the high concentration of H(2)O(2)-generating oxidases in peroxisomes and their set of antioxidant enzymes, especially catalase. Still, mitochondria have been very much placed in the centre of ROS metabolism and oxidative stress. This review discusses novel findings concerning the relationship between ROS and peroxisomes, as they revealed to be a key player in the dynamic spin of ROS metabolism and oxidative injury. An overview of ROS generating enzymes as well as their antioxidant counterparts will be given, exemplifying the precise fine-tuning between the opposing systems. Various conditions in which the balance between generation and scavenging of ROS in peroxisomes is perturbed, for example, exogenous manipulation, ageing and peroxisomal disorders, are addressed. Furthermore, peroxisome-derived oxidative stress and its effect on mitochondria (and vice versa) are discussed, highlighting the close interrelationship of both organelles.

Induction of oxidative stress and related transcriptional effects of perfluorononanoic acid using an in vivo assessment

“…Increased hydrogen peroxide (H 2 O 2 ) production due to exaggerated fatty acid β-oxidation may be harmful for the organism (Bonekamp et al, 2009). These may cause deleterious cellular effects, such as cell death and other pathological conditions, as a result of ROS produced during chemical or oxidative stress conditions (Bonekamp et al, 2009).…”

“…These may cause deleterious cellular effects, such as cell death and other pathological conditions, as a result of ROS produced during chemical or oxidative stress conditions (Bonekamp et al, 2009). An adaptation during limited oxygen conditions requires the induction of antioxidant and associated enzymes, such as CAT, SOD and GPx, in order to reduce potential damage during oxygen reintroduction.…”

Adiponectin inhibits oxidative stress in human prostate carcinoma cells

“…Owing to the presence and action of xanthine oxidase, peroxisomal ROS consist predominantly of superoxide anion radicals. 20 Adiponectin has been shown to activate 5 0 AMP-activated protein kinase (AMPK). [21][22][23] Activated AMPK phosphorylates and inactivates the main regulator of mitochondrial fatty acid oxidation acetyl-CoA carboxylase (ACC).…”

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“…During physiological homeostasis overall oxidative balance is maintained by the removal of ROS via a variety of antioxidants to match the production of ROS from a variety of sources. 6 Overproduction of ROS or lack of antioxidants leads to oxidative stress and cause oxidative damage such as …”

“…During physiological homeostasis overall oxidative balance is maintained by the removal of ROS via a variety of antioxidants to match the production of ROS from a variety of sources. 6 Overproduction of ROS or lack of antioxidants leads to oxidative stress and cause oxidative damage such as deleterious cellular effects, cell death, and diverse pathological conditions. One major contributor to oxidative damage is hydrogen peroxide (H 2 O 2 ), which is produced from superoxide that leaks from the mitochondria.…”