Essa Musthafa Mohamed, Subash Selvaraju, Braidy Nady, Al-Adawi Samir, Lim Chai K, Manivasagam Tamilarasan, Guillemin Gilles J
Dept of Food Science and Nutrition, College of Agriculture and Marine Sciences, Sultan Qaboos University, Oman. ; School of Medical Sciences, Department of Pharmacology, Faculty of Medicine, University of NSW, Sydney, Australia.
Int J Tryptophan Res. 2013 Jul 21;6(Suppl 1):15-28. doi: 10.4137/IJTR.S11355. Print 2013.
Autism spectrum disorder (ASD) is a pervasive neuro-developmental disorder characterized by impaired social interaction, reduced/absent verbal and non-verbal communication, and repetitive behavior during early childhood. The etiology of this developmental disorder is poorly understood, and no biomarkers have been identified. Identification of novel biochemical markers related to autism would be advantageous for earlier clinical diagnosis and intervention. Studies suggest that oxidative stress-induced mechanisms and reduced antioxidant defense, mitochondrial dysfunction, and impaired energy metabolism (NAD(+), NADH, ATP, pyruvate, and lactate), are major causes of ASD. This review provides renewed insight regarding current autism research related to oxidative stress, mitochondrial dysfunction, and altered tryptophan metabolism in ASD.
自闭症谱系障碍(ASD)是一种广泛性神经发育障碍,其特征为社交互动受损、言语和非言语交流减少/缺失,以及幼儿期的重复行为。这种发育障碍的病因尚不清楚,尚未发现生物标志物。识别与自闭症相关的新型生化标志物将有助于早期临床诊断和干预。研究表明,氧化应激诱导机制、抗氧化防御能力降低、线粒体功能障碍以及能量代谢受损(NAD(+)、NADH、ATP、丙酮酸和乳酸)是ASD的主要病因。本综述为当前与ASD中氧化应激、线粒体功能障碍和色氨酸代谢改变相关的自闭症研究提供了新的见解。