Comparison of taurine, GABA, Glu, and Asp as scavengers of malondialdehyde in vitro and in vivo
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NANO EXPRESS
Open Access
Comparison of taurine, GABA, Glu, and Asp as scavengers of malondialdehyde in vitro and in vivo Yan Deng1,2*†, Wei Wang1†, Pingfeng Yu3, Zhijiang Xi2, Lijian Xu1, Xiaolong Li1,2 and Nongyue He1,2*
Abstract The purpose of this study is to determine if amino acid neurotransmitters such as gamma-aminobutyric acid (GABA), taurine, glutamate (Glu), and aspartate (Asp) can scavenge activated carbonyl toxicants. In vitro, direct reaction between malondialdehyde (MDA) and amino acids was researched using different analytical methods. The results indicated that scavenging activated carbonyl function of taurine and GABA is very strong and that of Glu and Asp is very weak in pathophysiological situations. The results provided perspective into the reaction mechanism of taurine and GABA as targets of activated carbonyl such as MDA in protecting nerve terminals. In vivo, we studied the effect of taurine and GABA as antioxidants by detecting MDA concentration and superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities. It was shown that MDA concentration was decreased significantly, and the activities of SOD and GSH-Px were increased significantly in the cerebral cortex and hippocampus of acute epileptic state rats, after the administration of taurine and GABA. The results indicated that the peripherally administered taurine and GABA can scavenge free radicals and protect the tissue against activated carbonyl in vivo and in vitro. Keywords: Taurine, Gamma-aminobutyric acid, Glutamate, Aspartate, Scavengers, Malondialdehyde
Background There is a common character for all neurodegenerative diseases: all of which, such as Parkinson's disease (PD) and Alzheimer's disease (AD), are connected with neuronal apoptosis induced by oxidative stress and carbonyl stress [1,2]. Oxidative injury plays a role in the initiation and progression of epilepsy [3]. In pathophysiological situations of the brain, the high metabolic rate, low concentration of glutathione and antioxidant enzyme catalase, and high proportion of polyunsaturated fatty acids make the brain tissue and DNA particularly susceptible to oxidative and carbonyl damage causing neurodegenerative disorders [4-6]. The Maillard reaction and advanced lipid
* Correspondence: [email protected]; [email protected] † Equal contributors 1 Hunan Key Laboratory of Green Packaging and Application of Biological Nanotechnology, Hunan University of Technology, Zhuzhou, 412007, People’s Republic of China 2 State Key Laboratory of Bioelectronics, Southeast University, Nanjing, 210096, People’s Republic of China Full list of author information is available at the end of the article
peroxidation reactions lead to the formation of advanced glycation end products (AGEs) and advanced lipoxidation end products (ALEs), whose processes have been widely documented to be responsible for the formation of various age pigment-like fluorophores and many chronic diseases, such as neuronal degenerative diseases, chronic fatigue syndrome, and physiological aging [7-1
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