Mitochondrial toxins potentiate hydroxyl radical production in rat striatum during carbon monoxide poisoning.

Abstract

Hydroxyl radical (•OH) production in the rat striatum during carbon monoxide (CO) poisoning, which inhibits complex IV, was enhanced synergistically by malonate, a mitochondrial complex II inhibitor, but not N-methyl-4-phenylpyridinium or NaCN, complex I and IV inhibitors, respectively. No such enhancement appeared in the case of NaCN combined with malonate. Intrastriatal dopamine, which is involved in •OH production by malonate, did not synergistically enhance CO-induced •OH production. Diphenyleneiodonium, a nonselective NADPH oxidase inhibitor, partly suppressed the potentiation of CO-induced •OH production by malonate. Impairment of mitochondrial functions might potentiate oxidative stress and intensify CO toxicity in the brain.

• Authors: Fumi Kuriiwa, Masamune Kobayashi, Hajime Mizukami, Shuichi Hara
• Journal: Journal of pharmacological sciences (J Pharmacol Sci) Vol. 146 Issue 1 Pg. 29-32 (May 2021) ISSN: 1347-8648 [Electronic] Japan
• PMID: 33858652 (Publication Type: Journal Article)
• Copyright: Copyright © 2021 The Authors. Production and hosting by Elsevier B.V. All rights reserved.

Chemical References

• Enzyme Inhibitors
• Malonates
• Onium Compounds
• Hydroxyl Radical
• diphenyleneiodonium
• malonic acid
• NADPH Oxidases
• Electron Transport Complex IV

Topics

• Animals
• Carbon Monoxide Poisoning (metabolism)
• Corpus Striatum (metabolism)
• Electron Transport Complex IV (antagonists & inhibitors)
• Enzyme Inhibitors (pharmacology)
• Hydroxyl Radical (metabolism)
• Male
• Malonates (pharmacology)
• Mitochondria (metabolism)
• NADPH Oxidases (antagonists & inhibitors)
• Onium Compounds (pharmacology)
• Oxidative Stress (drug effects)
• Rats, Sprague-Dawley