GSTM2

Last update 08 May 2025

Basic Info

Synonyms

glutathione S-transferase mu 2, GST class-mu 2, GST4

+ [2]

Introduction

Conjugation of reduced glutathione to a wide number of exogenous and endogenous hydrophobic electrophiles. Participates in the formation of novel hepoxilin regioisomers (PubMed:21046276).

100 Clinical Results associated with GSTM2

100 Translational Medicine associated with GSTM2

0 Patents (Medical) associated with GSTM2

421

Literatures (Medical) associated with GSTM2

01 Jun 2025·Biogerontology

Vorinostat, a potential hormetin, extends lifespan and enhances stress resistance via the SKN-1 pathway in Caenorhabditis elegans

Article

Author: Huang, Shuai ; Shi, Zhidan ; He, Ling ; Wu, Jiawei ; Shi, Hang

Vorinostat, a pan histone deacetylases (HDACs) inhibitor clinically approved for cutaneous T-cell lymphoma, exerts therapeutic effects by inducing tumor cell death and cycle arrest. Intriguingly, a previously unrecognized hormetic role of low-dose vorinostat in Caenorhabditis elegans. Subtoxic concentrations of vorinostat (1 μM) significantly extended lifespan, enhanced healthspan, and improved resistance to oxidative and heat stress, while ameliorating Aβ-induced paralysis. qPCR analysis demonstrated dose-dependent bidirectional regulation of stress-resistance genes (sod-3, hsp-16.2, skn-1, gst-4, act-1), with low doses of vorinostat upregulating these genes whereas higher doses (10 μM) exerted suppressive or neutral effects. Mechanistically, vorinostat-induced hormesis required functional SKN-1 signaling, as evidenced by its capacity to activate skn-1 and downstream targets (hsp-16.2, gst-4, act-1). Crucially, RNAi-mediated skn-1 knockdown completely abolished the pro-longevity and stress-resistant phenotypes. These findings establish vorinostat as a novel hormetin that enhances organismal resilience through SKN-1 pathway activation, providing new insights into HDAC inhibitor biology and aging intervention strategies.

01 May 2025·Journal of Ethnopharmacology

Niuhuang jiedu prescription alleviates realgar-induced dopaminergic and GABAergic neurotoxicity in Caenorhabditis elegans

Article

Author: Chen, Xiaowei ; Wang, Ying ; Zhu, Jiansheng ; Zou, Lingyue ; Li, Guochun ; Ruan, Qinli ; Dong, Ju ; Du, Linjuan

ETHNOPHARMACOLOGICAL RELEVANCENiuhuang Jiedu (NHJD) is a Chinese medicine prescription containing realgar (As₂S₂), which is neurotoxic, and seven other traditional Chinese medicines (TCMs). However, whether the multiple TCMs contained in NHJD can mitigate the neurotoxicity of realgar is yet to be elucidated.AIM OF THE STUDYThis study aimed to investigate the effect of NHJD on realgar-induced neurotoxicity and elucidate its underlying mechanisms.MATERIAL AND METHODSCaenorhabditis elegans was treated with realgar suspension (1-8 mg/mL) for 48 h. Transgenic nematode strains labeled with green fluorescent protein were used to evaluate neuronal structural damage. Locomotion and perception behaviors were assessed by measuring head thrashes, body bends, and chemotaxis. Oxidative stress was determined by detecting reactive oxygen species (ROS), lipofuscin, and glutathione-S-transferase-4 (GST-4) levels. Subsequently, a quantitative reverse transcription-polymerase chain reaction was employed to analyze gene expression associated with oxidative stress, whereas the role of the p38 MAPK pathway was investigated using KU25 nematodes. Finally, arsenic species in the nematodes were estimated using high-performance liquid chromatography-atomic fluorescence spectrometry. Data analysis was performed using analysis of variance or rank tests with SPSS 26.0.RESULTSTreatment of nematodes with 8 mg/mL realgar resulted in significant damage to dopaminergic and GABAergic neurons, impaired locomotor and perceptual behavior (at 4-8 mg/mL), and induced oxidative damage (at 2-8 mg/mL). A neuron-defective model was established using 8 mg/mL realgar to gauge the effects of NHJD on realgar-induced damage. The findings indicated that NHJD, containing the same dose of realgar, significantly alleviated neuronal damage and neurobehavioral impairment and increased ROS, lipofuscin, and GST-4 levels. In addition, NHJD reduced the expressions of oxidative stress-related genes (gst-4, skn-1, gcs-1, gss-1, ctl-2, ctl-3, and sod-1) compared with realgar alone. Nonetheless, significant differences in skn-1 expression, neurobehavior, ROS, or lipofuscin levels were not observed between the realgar and NHJD groups in KU25 nematodes. Moreover, arsenic methylation metabolites were not identified in the nematodes.CONCLUSIONSThe multiple TCMs contained in NHJD effectively mitigated realgar-induced dopaminergic and GABAergic neurotoxicity in nematodes, and pmk-1 may play a crucial role in NHJD's alleviating realgar-induced neurotoxicity via the p38 MAPK signaling pathway.

01 May 2025·Ecotoxicology and Environmental Safety

Chlorantraniliprole-induced oxidative stress, DNA damage, and apoptosis in Caenorhabditis elegans: Mechanistic insights and ecological risk implications

Article

Author: Hu, Guokun ; Ji, Xiaoxue ; Han, Shaohua ; Qiao, Kang ; Yang, Mengzhen ; Hu, Fengyuan

Chlorantraniliprole (CAP) is one of the most widely used insecticides in the world. CAP is strictly restricted in foodstuff with maximum residual limits (MRLs) from 0.01 to 40 mg/kg set by Chinese national food safety standard. However, a detailed evaluation on its possible acute toxicity and the underlying mechanisms remains inconclusive. In this study, effects of CAP at environmentally relevant concentrations on growth, locomotion, lifespan, reproduction, and antioxidative defense systems were evaluated using the model organism Caenorhabditis elegans. Exposure to CAP notably reduced nematode development, head thrash, and pharyngeal pumping frequency compared with the control. Moreover, CAP at 0.1, 1, and 10 μg/L decreased lifespan of nematodes by 23.73 %, 28.71 %, and 36.23 %, respectively. CAP at 1 and 10 μg/L enhanced the ROS level, reduced the activity of antioxidative enzyme, including CAT and SOD. CAP also regulated mRNA expression levels of daf-16, skn-1, sod-3, gst-4, ced-3, ced-4, ced-9, egl-1, clk-2, and hus-1 in the nematodes, while no significant effect in the mutants was observed. Pearson correlation analysis revealed that significant correlation existed between tested parameters, indicating that CAP caused a series of negative effects in the nematodes. Meanwhile, molecular docking results revealed the potential of CAP to bind with oxidative stress, DNA damage and apoptosis proteins, providing molecular mechanisms for the observed detrimental effects. Therefore, our results suggested that acute exposure to CAP at environmental concentrations caused oxidative stress, DNA damage and apoptosis in the nematodes. Our results shed new light on risk assessment and management of CAP.

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GSTM2

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