Lam PY, Chen N, Chiu PY, Leung HY, Ko KM
Division of Life Science, Hong Kong University of Science and Technology, Hong Kong SAR, China.
High levels of reactive oxygen species inflict oxidative damage on various cellular components that eventually culminate in a variety of diseases. This study investigated the cytoprotective effects of a nucleic acid-based health product (Squina [Hong Kong, China] DNA) against oxidative stress, particularly in neuronal cells. Adult female Sprague-Dawley rats were treated with Squina DNA, and changes in mitochondrial antioxidant status and functional capacity were assessed by the activities of antioxidant enzymes and ATP generation capacity in brain, heart ventricular, kidney, skeletal muscle, and liver tissues of control and Squina DNA-treated rats. The effects of Squina DNA pretreatment on brain/neuronal cell injury were investigated in a rat model of cerebral ischemia/reperfusion (I/R) injury and a neuroblastoma SH-SY5Y cell model of beta-amyloid (A-beta) protein fragment 25-35-induced toxicity. Long-term Squina DNA treatment caused dose-dependent increases in mitochondrial antioxidant status and functional capacity in rat brain, heart ventricular, kidney, skeletal muscle, and liver tissues. Squina DNA pretreatment significantly prevented I/R injury in brain tissue. The cerebroprotection was associated with a reversal of I/R-induced impairment in mitochondrial antioxidant status and disruption in membrane integrity. Squina DNA ethanol extract also significantly inhibited the A-beta-induced apoptosis in SH-SY5Y neuronal cells, as evidenced by less caspase 3 and caspase 9 activation as well as mitochondrial cytochrome c release in A-beta-challenged cells. Squina DNA may enhance the resistance of tissues and cells to oxidative stress, particularly in pathological conditions such as stroke and aging-related neurodegenerative diseases.