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 . 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 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 [7–11]. A variety of reactive carbonyl intermediates derived from Maillard and lipid peroxidation reactions acts as intermediates in the formation of AGEs and ALEs [12, 13]. These carbonyl compounds were found to react readily with an amino group of proteins with the formation of protein aggregates, resulting in protein structural and functional alterations .
Malondialdehyde (MDA) is the well-studied intermediate of oxidative stress . These reactive unsaturated carbonyls can target a variety of biological components, such as structural and functional proteins and nucleic acids [7, 16]. MDA causes tissue injury and the depression of energy metabolism, thus representing biochemical markers for disease progression and lipid peroxidation, such as Huntington's disease , familial amyotrophic lateral sclerosis (ALS) , AD, and vascular dementia [19, 20]. Recent research results suggest that schizophrenic patients exhibit increased MDA levels, which lead to neuronal damage . ALEs such as MDA have been implicated in the neuronal loss observed in a variety of neuropathological cases including AD, ALS, PD, and ischemia [2, 16, 22]. These findings further support a role of carbonyl injury in the pathogenesis and the potential benefits of antioxidant therapy .
Taurine (2-aminoethanesulfonic acid) and gamma-aminobutyric acid (GABA) are both natural amino acids with wide occurrence. In the context of the neural system, taurine and GABA are inhibitory amino acid neurotransmitters, and glutamate and aspartate are excitatory amino acids. Taurine was originally described to inhibit lipid peroxidation . At present, taurine has been demonstrated to protect the brain against lipid peroxidation and oxidative stress [25, 26]. It has also been shown that GABA exhibits anti-hypertensive effect, activates the blood flow, and increases the oxygen supply in the brain to enhance metabolic function of brain cells . Evidence suggests GABA-improved visual cortical function in senescent monkeys . Decreased proportion of GABA associated with age-related degradation of neuronal function and neuronal degenerative diseases . Recent study showed GABA-alleviated oxidative damage . Glutamate (Glu) and aspartate (Asp) are reported to prevent cardiac toxicity by alleviating oxidative stress . In this paper, it is hypothesized that several amino acids may inhibit the formation of ALEs and scavenge reactive carbonyl compounds such as MDA based on a potential carbonyl-amine reaction under physiological conditions, and its function is in vitro compared; also, the strong inhibition function of amino acids was investigated in vivo.