Abstract
The omega class glutathione S-transferases (GSTOs) are multifunctional enzymes involved in cellular defense and have distinct structural and functional characteristics, which differ from those of other GSTs. Previous studies provided evidence for the neuroprotective effects of GSTOs. However, the molecular mechanisms underpinning the neuroprotective functions of GSTOs have not been fully elucidated. Recently, our genetic and molecular studies using the Drosophila system have suggested that GstO1 has a protective function against H2O2-induced neurotoxicity by regulating the MAPK signaling pathway, and GstO2 is required for the activation of mitochondrial ATP synthase in the Drosophila neurodegenerative disease model. The comprehensive understanding of various neuroprotection mechanisms of Drosophila GstOs from our studies provides valuable insight into the neuroprotective functions of GstOs in vivo. In this review, we briefly introduce recent studies and summarize the novel biological functions and mechanisms underpinning neuroprotective effects of GstOs in Drosophila.
Highlights
Glutathione S-transferases (GSTs) are a superfamily of multifunctional isoenzymes involved in the cellular detoxification of several endogenous and exogenous compounds
Various studies suggest that oxidative stress plays an important role in the pathogenesis of several human diseases, including neurodegenerative diseases, the exact mechanism of GSTOs in neuroprotective effects against several oxidative stressors that provide a pharmacological basis for the relationship between GstOs and the development of neurodegenerative diseases has not been elucidated
GstO1 has a protective function against H2O2-induced neurotoxicity by regulating the MAPK signaling pathway
Summary
Glutathione S-transferases (GSTs) are a superfamily of multifunctional isoenzymes involved in the cellular detoxification of several endogenous and exogenous compounds. In vitro studies have shown that human GSTO1 participates in modulation of the ryanodine receptor, Oxidative Medicine and Cellular Longevity which is a Ca2+ release channel. These studies showed that human GSTO1 is involved in modulation of the signaling pathway during c-Jun N-terminal kinase(JNK-) mediated apoptosis and in the activation of interleukin-1β, an important mediator of inflammatory response [15,16,17]. An important role for human GSTO1-1 in glutathionylation of the target proteins has been described [17, 20]. GSTOs play important roles in decreasing oxidative stress produced by various stressors and cellular processes. We mainly focus on recent studies that have investigated the neuroprotective functions of GSTOs in the Drosophila model system
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