Determination of glutathione and glutathione disulfide using glutathione reductase and 2-vinylpyridine

Griffith, Owen W.

doi:10.1016/0003-2697(80)90139-6

Cited by 4,213 publications

(1,933 citation statements)

References 22 publications

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“…2A, within 30 min after BU treatment, the intracellular levels of GSH were reduced by 50%. This finding was subsequently confirmed by an enzymatic assay using glutathione reductase and 2-vinylpyridine [29]. The reduction in GSH sustained for about 2 h and then gradually lessened.…”

Section: Bu Induces a Transient Reduction In Gsh But A Continuous Incmentioning

confidence: 57%

Busulfan-induced senescence is dependent on ROS production upstream of the MAPK pathway

Probin

Wang

Zhou

2007

Free Radical Biology and Medicine

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Induction of cellular senescence is a common response of a normal cell to a DNA damaging agent, which may contribute to cancer chemotherapy-and ionizing radiation-induced normal tissue injury. The induction has been largely attributed to the activation of p53. However, the results from the present study suggest that busulfan (BU), an alkylating agent that causes DNA damage by crosslinking DNAs and DNA and proteins, induces senescence in normal human diploid WI38 fibroblasts through the extracellular signal-regulated kinase (Erk) and p38 mitogen-activated protein kinase (p38 MAPK) cascade independent of the p53-DNA damage pathway. The induction of WI38 cell senescence is initiated by a transient depletion of intracellular glutathione (GSH) and followed by a continuous increase in reactive oxygen species (ROS) production via nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, which leads to the activation of the Erk and p38 MAPK pathway. Incubation of WI38 cells with N-acetyl-cysteine (NAC) replenishes intracellular GSH; abrogates the increased production of ROS; ameliorates Erk and p38 MAPK activation; and attenuates senescence induction by BU. Thus, inhibition of senescence induction using a potent antioxidant or specific inhibitor of the Erk and p38 MAPK pathway has the potential to be developed as a mechanism-based strategy to ameliorate cancer therapy-induced normal tissue damage.

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Section: Bu Induces a Transient Reduction In Gsh But A Continuous Incmentioning

confidence: 57%

Busulfan-induced senescence is dependent on ROS production upstream of the MAPK pathway

Probin

Wang

Zhou

2007

Free Radical Biology and Medicine

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“…Experiments were performed using Swiss male mice 6-8 weeks old, weighing [20][21][22][23][24][25] g. The animals were fed standard pellet diet with vitamins, antibiotic and water were given ad libitum and housed in polypropylene cage (Tarson) in the departmental animal house with 12 h light:dark cycle under standard temperature [(25暲2) 曟 ]. The animals were allowed to acclimatize for one week.…”

Section: Animalsmentioning

confidence: 99%

“…Tissues were homogenized in the ice-cold buffer containing 0.25 M sucrose, 1 mM EDTA, and 1 mM Tris-HCl, pH 7.4. The homogenate was first centrifuged at 600 g for 10 min at 4 曟 , and the supernatant fractions were collected and further centrifuged at 8 000 g for 20 7.4 and stored at -80 曟 for the biochemical estimation of different parameters.…”

Section: Isolation Of Tissue Mitochondriamentioning

confidence: 99%

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Antioxidative effect of folate–modified chitosan nanoparticles

Chakraborty

Mahapatra

Sahu

et al. 2011

Asian Pacific Journal of Tropical Biomedicine

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“…For the GSSG assay, acid extract was treated with 2-vinylpyridine and triethanolamine as previously described [16], and the treated supernatant was used in the assay [15]. 7GCS activity was measured by the method described by Seelig and Meister [17].…”

Section: Gsh Gssg and ?Gcs Activity Assaysmentioning

confidence: 99%

Induction of γ‐glutamylcysteine synthetase by cigarette smoke is associated with AP‐1 in human alveolar epithelial cells

Rahman¹,

Smith

Lawson³

et al. 1996

FEBS Letters

152

117

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Increased levels of glutathione (GSH) occur in the epithelial lining fluid (ELF) of chronic cigarette smokers. Therefore we investigated the effect of cigarette smoke condensate solution (CSC) on GSH synthesis and the regulation of T-glutamylcysteine synthetase (~CS) in human type II alveolar epithelial cells (A549). CSC exposure increased GSH levels, TGCS activity and ~CS heavy subunit (HS) mRNA, as well as increasing DNA binding of the activator protein-1 (AP-1) and the human antioxidant response element (hARE). Transfection of deletion constructs of the ~GCS-HS promoter in a chloramphenicol acetyl transferase (CAT) reporter system revealed that an hARE, present within promoter, is not required tot the CSC mediated induction. We conclude that CSC induction of ~GCS-HS expression is associated with AP-1/AP-I-like responsive elements.

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Determination of glutathione and glutathione disulfide using glutathione reductase and 2-vinylpyridine

Cited by 4,213 publications

References 22 publications

Busulfan-induced senescence is dependent on ROS production upstream of the MAPK pathway

Busulfan-induced senescence is dependent on ROS production upstream of the MAPK pathway

Antioxidative effect of folate–modified chitosan nanoparticles

Induction of γ‐glutamylcysteine synthetase by cigarette smoke is associated with AP‐1 in human alveolar epithelial cells

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