Metabolic pathways in mammalian peroxisomes

doi:10.1016/0300-9084(93)90072-Z

Biochimie

Volume 75, Issues 3–4, 1993, Pages 147-158

https://doi.org/10.1016/0300-9084(93)90072-Z Get rights and content

Abstract

This article summarizes our current knowledge of the metabolic pathways present in mammalian peroxisomes. Emphasis is placed on those aspects that are not covered by other articles in this issue: peroxisomal enzyme content and topology; the peroxisomal β-oxidation system; substrates of peroxisomal β-oxidation such as very-long-chain fatty acids, branched fatty acids, dicarboxylic fatty acids, prostaglandins and xenobiotics; the role of peroxisomes in the metabolism of purines, polyamines, amino acids, glyoxylate and reactive oxygen products such as hydrogen peroxide, superoxide anions and epoxides.

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They have been named as peroxisomes owing to their participation in hydrogen peroxide generating and scavenging pathways (De Duve and Baudhuin, 1966). Peroxisomes contain a host of oxidative enzymes, more than half of which are involved in the degradation of fatty acids and cholesterol via β-oxidation (Mannaerts and Van, 1993). In mammals, they are also involved in plasmalogen biosynthesis, synthesis of bile acids, and neuronal function modulators like docosahexaenoic acid (DHA) and degradation of leukotrienes (Wanders and Waterham, 2006; Jedlitschky et al., 1993)
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This data suggests that peroxisomes are highly abundant in the murine parotid gland and might help to protect against oxidative stress. This comprehensive description of peroxisomes in the parotid gland lays the groundwork for further research concerning their role in the pathogenesis of parotid gland diseases and tumors.
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Reactive oxygen species (ROS) are thought to be a major driving force in human aging, disease, and carcinogenesis, and arise from both endogenous and exogenous sources. Normal cellular metabolism via oxidative phosphorylation by mitochondria [1], breakdown of long chain fatty acids by peroxisomes [2], and defense mechanisms employed by inflammatory cells (e.g., neutrophils, eosinophils, and macrophages) [3] are major sources of endogenous ROS. Ionizing radiation (IR), ultraviolet (UV) light, chemicals agents in food and the environment, and chemotherapeutics are exogenous agents that can induce ROS formation either through direct or indirect mechanisms.
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