Department of Biochemistry, Faculty of Veterinary Medicine, Alexandria University, Edfina, 22758, Egypt.
Department of Biochemistry, Faculty of Veterinary Medicine, Damanhour University, Damanhour, 22511, Egypt.
Metab Brain Dis. 2017 Oct;32(5):1639-1647. doi: 10.1007/s11011-017-0052-y. Epub 2017 Jun 28.
A significant association between fructose corn syrup in sweetened beverages consumption and increased risk of detrimental central nervous system effects has been recently reported. We hypothesized that the aspartame and soft drink induced disturbances in energy production and endocrine function, which play a role in the induction of brain damage. Therefore, we aimed to assess the effect of aspartame and soft drink on brain function and the link between energy status in the brain, oxidative stress and molecular pathways of apoptosis. Thirty rats were randomly assigned to drink water, aspartame (240 mg/kg orally) and cola soft drinks (free access) daily for two months. Subchronic intake of aspartame and soft drink significantly disrupted the brain energy production, as indicated by inhibited serum and brain creatine kinase, specifically in soft drink-received rats. Moreover, they substantially altered serum electrolytes (increased Ca and Na, and depleted Cu, Fe, Zn and K levels), and accordingly the related hormonal status (increased T4 and PTH, and lowered T3 and aldosterone levels), particularly in soft drink-received rats reflecting brain damage. Additionally, significant increment of acetylcholine esterase activity concomitant with the reduction of antioxidant molecules (SOD, CAT, GSH-Px and GSH), and induction of malondialdehyde level are precisely indicative of oxidative brain damage. Brain mRNA transcripts of target genes showed that aspartame and soft drink induced upregulation of BAX, Casp3, P27 and Mdm2 (1.5-fold) and down-regulation of Bcl2, suggesting an activation of cellular apoptosis. Collectively, subchronic aspartame and soft drink-induced brain damage in rats may be driven via a mechanism that involves energy production disruption, electrolytes and hormonal imbalance, increased oxidative stress and activation of molecular pathway of neuronal apoptosis.
最近有研究报道称，在含糖饮料中摄入果葡糖浆与中枢神经系统不良影响风险增加之间存在显著关联。我们假设阿斯巴甜和软饮料会引起能量产生和内分泌功能紊乱，而这些紊乱在诱导脑损伤中起作用。因此，我们旨在评估阿斯巴甜和软饮料对大脑功能的影响，以及大脑能量状态、氧化应激和细胞凋亡分子途径之间的联系。
将 30 只大鼠随机分为三组，分别饮用水、阿斯巴甜（240mg/kg 口服）和可乐软饮料（自由饮用），持续两个月。亚慢性摄入阿斯巴甜和软饮料会显著破坏大脑的能量产生，表现为血清和大脑肌酸激酶受到抑制，尤其是在饮用软饮料的大鼠中。此外，它们还会显著改变血清电解质（增加 Ca 和 Na，耗尽 Cu、Fe、Zn 和 K 水平），并相应地改变相关激素状态（增加 T4 和 PTH，降低 T3 和醛固酮水平），特别是在饮用软饮料的大鼠中，这反映了脑损伤。
此外，乙酰胆碱酯酶活性的显著增加伴随着抗氧化分子（SOD、CAT、GSH-Px 和 GSH）的减少，以及丙二醛水平的升高，这些都精确地表明了氧化应激导致的脑损伤。大脑靶基因的 mRNA 转录显示，阿斯巴甜和软饮料诱导 BAX、Casp3、P27 和 Mdm2 的上调（1.5 倍）和 Bcl2 的下调，提示细胞凋亡途径的激活。
总之，亚慢性摄入阿斯巴甜和软饮料导致的大鼠脑损伤可能是通过破坏能量产生、电解质和激素失衡、增加氧化应激和激活神经元细胞凋亡分子途径的机制来驱动的。
