The neuroprotective effects of taurine against nickel by reducing oxidative stress and maintaining mitochondrial function in cortical neurons. (17th March 2015)

• Record Type: Journal Article
• Authors: Xu, Shangcheng; He, Mindi; Zhong, Min; Li, Li; Lu, Yonghui; Zhang, Yanwen; Zhang, Lei; Yu, Zhengping; Zhou, Zhou
• Is Part Of: Neuroscience letters. Volume 590(2015)
• Page Start: 52
• Page End: 57
• Publication Date: 2015-03-17
• Subjects: ATP adenosine-5′-triphosphate -- LDH lactate dehydrogenase -- MDA malondialdehyde -- SOD superoxide dismutase -- GSH glutathione -- GSSG glutathione oxide -- mtDNA mitochondrial DNA -- ROS reactive oxygen species -- ΔΨm mitochondrial membrane potential; Nickel -- Taurine -- Neurotoxicity -- Oxidative stress -- Mitochondria; Neurology -- Periodicals; Neurology -- Periodicals; Research -- Periodicals; Neurologie -- Périodiques; Neuroanatomie -- Périodiques; Neuropharmacologie -- Périodiques; Neurophysiologie -- Périodiques; Neurology; Periodicals; Electronic journals; 617.48
• DOI: 10.1016/j.neulet.2015.01.065
• Languages: English
• ISSNs: 0304-3940

Abstract

Highlights: Taurine diminished nickel-induced cytotoxicity in primary cultured neurons. Taurine attenuated the oxidative stress and mitochondrial dysfunction of neurons exposed to nickel. Taurine may have pharmacological potential in treating the adverse effects of neurotoxins that target the mitochondria. Abstract: Previous studies have indicated that oxidative stress and mitochondrial dysfunction are involved in the toxicity of nickel. Taurine is recognized as an efficient antioxidant and is essential for mitochondrial function. To investigate whether taurine could protect against the neurotoxicity of nickel, we exposed primary cultured cortical neurons to various concentrations of nickel chloride (NiCl2 ; 0.5 mM, 1 mM and 2 mM) for 24 h or to 1 mM NiCl2 for various periods (0 h, 12 h, 24 h and 48 h). Our results showed that taurine efficiently reduced lactate dehydrogenase (LDH) release induced by NiCl2 . Along with this protective effect, taurine pretreatment not only significantly reversed the increase of ROS production and mitochondrial superoxide concentration, but also attenuated the decrease of superoxide dismutase (SOD) activity and glutathione (GSH) concentration in neurons exposed to NiCl2 for 24 h. Moreover, nickel exposure reduced ATP production, disrupted the mitochondrial membrane potential and decreased mtDNA content. These types of oxidative damage in the mitochondria were efficiently ameliorated by taurine pretreatment. Taken together, our results indicate that the neuroprotective effects of taurine against the toxicity of nickel might largely depend on its roles in reducing oxidative stress and improving mitochondrial function. Taurine may have great pharmacological potential in treating the adverse effects of nickel in the nervous system.