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Chonnam Med J. 2018 Sep;54(3):159-166. doi: 10.4068/cmj.2018.54.3.159. Epub 2018 Sep 27.

Effects of NADPH Oxidase Inhibitors and Mitochondria-Targeted Antioxidants on Amyloid β.

Chonnam medical journal

Shinae Hwang, Jong-Keun Kim

Affiliations

  1. Department of Pharmacology, Chonnam National University Medical School, Hwasun, Korea.

PMID: 30288371 PMCID: PMC6165920 DOI: 10.4068/cmj.2018.54.3.159

Abstract

The Amyloid β peptide (Aβ) is a main component of senile plaques in Alzheimer's disease. Currently, NADPH oxidase (NOX) and mitochondria are considered as primary sources of ROS induced by Aβ. However, the contribution of NOX and mitochondria to Aβ-induced ROS generation has not been well defined. To delineate the relative involvement of NOX and mitochondria in Aβ-induced ROS generation and neuronal death in mouse cortical cultures, we examined the effect of NOX inhibitors, apocynin and AEBSF, and the mitochondria-targeted antioxidants (MTAs), mitotempol and mitoquinone, on Aβ-induced ROS generation and neuronal deaths. Cell death was assessed by measuring lactate dehydrogenase efflux in bathing media at 24 and 48 hrs after exposure to Aβ

Keywords: Amyloid Beta-Peptides; Mitochondria; NADPH Oxidase; Oxidative Stress

Conflict of interest statement

CONFLICT OF INTEREST STATEMENT: None declared.

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