Autism Research and Treatment Center, Riyadh, Saudi Arabia.
Shaik AL-Amodi Autism Research Chair, King Saud University, Riyadh, Saudi Arabia.
Food Nutr Res. 2016 Mar 3;60:28127. doi: 10.3402/fnr.v60.28127. eCollection 2016.
Abnormalities in fatty acid metabolism and membrane fatty acid composition play a part in a wide range of neurodevelopmental and psychiatric disorders. Altered fatty acid homeostasis as a result of insufficient dietary supplementation, genetic defects, the function of enzymes involved in their metabolism, or mitochondrial dysfunction contributes to the development of autism.
This study evaluates the association of altered brain lipid composition and neurotoxicity related to autism spectrum disorders in propionic acid (PA)-treated rats.
Forty-eight young male western albino rats were used in this study. They were grouped into six equal groups with eight rats in each. The first group received only phosphate buffered saline (control group). The second group received a neurotoxic dose of buffered PA (250 mg/kg body weight/day for 3 consecutive days). The third and fourth groups were intoxicated with PA as described above followed by treatment with either coenzyme Q (4.5 mg/kg body weight) or melatonin (10 mg/kg body weight) for 1 week (therapeutically treated groups). The fifth and sixth groups were administered both compounds for 1 week prior to PA (protected groups). Methyl esters of fatty acid were extracted with hexane, and the fatty acid composition of the extract was analyzed on a gas chromatography.
The obtained data proved that fatty acids are altered in brain tissue of PA-treated rats. All saturated fatty acids were increased while all unsaturated fatty acids were significantly decreased in the PA-treated group and relatively ameliorated in the pre-post melatonin and coenzyme Q groups.
Melatonin and coenzyme Q were effective in restoring normal level of most of the impaired fatty acids in PA-intoxicated rats which could help suggest both as supplements to ameliorate the autistic features induced in rat pups.
脂肪酸代谢和膜脂肪酸组成的异常在广泛的神经发育和精神疾病中起着一定的作用。由于饮食补充不足、遗传缺陷、参与其代谢的酶的功能或线粒体功能障碍导致脂肪酸动态平衡的改变，导致自闭症的发展。
本研究评估丙酸（PA）处理大鼠中与自闭症谱系障碍相关的改变的脑脂质组成和神经毒性之间的关系。
本研究使用了 48 只年轻雄性西部白化大鼠。它们被分为六组，每组 8 只。第一组仅接受磷酸盐缓冲生理盐水（对照组）。第二组连续 3 天每天接受神经毒性剂量的缓冲 PA（250mg/kg 体重）。第三和第四组如上所述用辅酶 Q（4.5mg/kg 体重）或褪黑素（10mg/kg 体重）治疗 1 周（治疗组）。第五和第六组在 PA 之前用两种化合物治疗 1 周（保护组）。用己烷提取脂肪酸的甲酯，并用气相色谱分析提取物的脂肪酸组成。
获得的数据证明了在 PA 处理的大鼠脑组织中脂肪酸发生了改变。所有饱和脂肪酸都增加了，而所有不饱和脂肪酸在 PA 处理组中都显著减少，在褪黑素和辅酶 Q 预处理组中相对改善。
褪黑素和辅酶 Q 在恢复 PA 中毒大鼠受损脂肪酸的正常水平方面是有效的，这可能有助于提示两者作为补充剂来改善幼鼠诱导的自闭症特征。
