The biochemistry of acetaminophen hepatotoxicity and rescue: a mathematical model PY2012 IR94 IR95

The biochemistry of acetaminophen hepatotoxicity and rescue: a mathematical model PY2012 IR94 IR95

##

Acetaminophen-induced hepatic necrosis. IV. Protective role of glutathione PY1973 IR94 IR95

##

##

Glutathione modulates Ca(2+) influx and oxidative toxicity through TRPM2 channel in rat dorsal root ganglion neurons; PY2011; Turkey (土耳其);_WJD_2022-0203_V001R01_IR95_

Glutathione modulates Ca(2+) influx and oxidative toxicity through TRPM2 channel in rat dorsal root ganglion neurons; PY2011; Turkey (土耳其);_WJD_2022-0203_V001R01_IR95_
--- -  - --- -  - ---
2022-02-03
Glutathione modulates Ca(2+) influx and oxidative toxicity through TRPM2 channel in rat dorsal root ganglion neurons; PY2011; Turkey (土耳其);_WJD_2022-0203_V001R01_IR95_RvD20220203_
Source or References (資訊來源或是參考資訊):
https://pubmed.ncbi.nlm.nih.gov/21748272/
Info cited on 2022-02-03-WD4 (資訊引用於 中華民國111年西元2022年2月3日) by 湯偉晉 (WeiJin Tang)
#

- -  - - - -  - -

J Membr Biol
. 2011 Aug;242(3):109-18. doi: 10.1007/s00232-011-9382-6. Epub 2011 Jul 12.

Glutathione modulates Ca(2+) influx and oxidative toxicity through TRPM2 channel in rat dorsal root ganglion neurons

Mustafa Nazıroğlu 1, Cemil Özgül, Bilal Çiğ, Salih Doğan, Abdulhadi Cihangir Uğuz
Affiliations collapse
Affiliation
1Department of Biophysics, Faculty of Medicine, University of Süleyman Demirel, 32260 Isparta, Turkey. mnaziroglu@med.sdu.edu.tr
PMID: 21748272 DOI: 10.1007/s00232-011-9382-6

Abstract
Glutathione (GSH) is the most abundant thiol antioxidant in mammalian cells and maintains thiol redox in the cells. GSH depletion has been implicated in the neurobiology of sensory neurons. Because the mechanisms that lead to melastatin-like transient receptor potential 2 (TRPM2) channel activation/inhibition in response to glutathione depletion and 2-aminoethyldiphenyl borinate (2-APB) administration are not understood, we tested the effects of 2-APB and GSH on oxidative stress and buthionine sulfoximine (BSO)-induced TRPM2 cation channel currents in dorsal root ganglion (DRG) neurons of rats. DRG neurons were freshly isolated from rats and the neurons were incubated for 24 h with BSO. In whole-cell patch clamp experiments, TRPM2 currents in the rat were consistently induced by H(2)O(2) or BSO. TRPM2 channels current densities and cytosolic free Ca(2+) content of the neurons were higher in BSO and H(2)O(2) groups than in control. However, the current densities and cytosolic Ca(2+) release were also higher in the BSO + H(2)O(2) group than in the H(2)O(2) alone. When intracellular GSH is introduced by pipette (吸管) TRPM2 channel currents were not activated by BSO, H(2)O(2) or rotenone (魚藤酮). BSO and H(2)O(2)-induced Ca(2+) gates were blocked by the 2-APB. Glutathione peroxidase activity, lipid peroxidation and GSH levels in the DRG neurons were also modulated by GSH and 2-APB inhibition. In conclusion, we observed the protective role of 2-APB and GSH on Ca(2+) influx through a TRPM2 channel in intracellular GSH depleted DRG neurons. Since cytosolic glutathione depletion is a common feature of neuropathic pain and diseases of sensory neuron, our findings are relevant to the etiology of neuropathology in DRG neurons.

#
Aminoethoxydiphenyl borate and flufenamic acid inhibit Ca2+ influx through TRPM2 channels in rat dorsal root ganglion neurons activated by ADP-ribose and rotenone (魚藤酮).

The decrease in hippocampal transient receptor potential M2 (TRPM2) channel and muscarinic acetylcholine receptor 1 (CHRM1) is associated with memory loss in a surgical menopause rat model.
Pala S, Atilgan R, Kuloglu T, Yalçın E, Kaya N, Etem E.

- - - - -- -- - -
--- --- -   - --- ---