Ethanol (ETOH) can cause apoptotic death of neurons by depleting GSH with an associated increase in oxidative stress. The current study illustrates a means to overcome this ETOH-induced neurotoxicity by enhancing GSH through boosting Nrf2, a transcription factor that controls GSH homeostasis. ETOH treatment caused a significant increase in Nrf2 protein, transcript expression, Nrf2-DNA binding a...

Arsenic trioxide (ATO; As2O3) induces cell death in various types of cancer cells including lung cancer via increasing reactive oxygen species (ROS) and regulating mitogen-activated protein kinase (MAPK) signaling cascades. However, little is known about the relationship between ATO and MAPK signaling in normal lung cells. Here, we investigated th...

Chronic ethanol feeding selectively impairs the translocation of cytosol GSH into the mitochondrial matrix. Since ethanol-induced liver cell injury is preferentially localized in the centrilobular area, we examined the hepatic acinar distribution of mitochondrial GSH transport in ethanol-fed rats. Enriched periportal (PP) and perivenous (PV) hepatocytes from pair- and ethanol-fed rats were prep...

Ifosfamide a clinically potent chemotherapeutic agent causes depletion of intracellular glutathione (GSH) levels in different cell types. GSH is the major intracellular reductant against oxidative stress. 4-hydroxyifosfamide (4-OH-IF), the activated form of ifosfamide, depletes GSH levels in T cells and NK cells which is accompanied by a decrease in T cell and NK function. Here we demonstrate f...

Because mitogen-activated protein kinases (MAPK) are downstream effectors of antioxidant responses, changes in GSH levels in an organism might induce organ-specific responses. To test our hypothesis, mice were treated intraperitoneally with L-buthionine-S-R-sulfoximine (BSO) to inhibit GSH synthesis. A time-related GSH depletion in the liver and kidney correlated with p38(MAPK) phosphorylation ...

Gallic acid (GA) found in various plants, fruits and foods has various biological effects including apoptosis. However, little is known about the relationship between reactive oxygen species (ROS) and p38 signaling in GA-treated endothelial cells (ECs). In this study, we investigated the effects of p38 inhibitor on GA-induced calf pulmonary artery endothelial cells (CPAEC) and human umbilical v...

Glutathione (GSH) is the most abundant cellular thiol playing an essential role in preserving a reduced cellular environment. Cellular GSH levels can be efficiently reduced by the GSH biosynthesis inhibitor, L-buthionine sulfoximine (BSO). The aim of our study was to determine the role of GSH in the growth of two C-cluster enteroviruses, poliovirus type 1 (PV1) and coxsackievirus A20 (CAV20). O...

Ifosfamide, a clinically potent chemotherapeutic agent, causes the depletion of intracellular glutathione (GSH) levels in various cell types. GSH is the major intracellular reductant against oxidative stress. 4-Hydroxyifosfamide (4-OH-IF), the activated form of ifosfamide, depletes GSH levels in T cells and natural killer (NK) cells; this is accompanied by a decrease in T-cell and NK-cell funct...

AIMS Chronic depletion of myocardial glutathione (GSH) may play a role in cardiac remodelling and dysfunction. This study examined the relationship between chronic GSH depletion and cardiac failure induced by pressure overload in mice lacking the modifier subunit (GCLM) of glutamate-cysteine ligase, the rate-limiting enzyme for GSH synthesis. In addition, we examined the association between idi...