Protective Effects Of Astaxanthin On Mitochondria Damage Induced By Reactive Oxygen Species

A large number of studies show that oxidative damage of mitochondria induced by excessive reactive oxygen species (ROS). Mitoehondria (especially damaged mitochondria) is the major intracellular organelle producing ROS. Mitochondrial membrane structure and function of the missing is relevant with many of the diseases.According to the literature, degenerative diseases, aging and cardiovascular disease are all related to mitochondrial dysfunction, which is mainly manifested in dysfunction:mitochondrial membrane potential, mitochondrial DNA (mtDNA) mutations, mitochondrial respiratory chainuncoupling, the free increased production of other base.At present, the antioxidant of astaxanthin, most of them focused on antioxidant enzymes activity and studies on the expression of enzymes in the oxidative damage of cells. But studies have reported the relatively few studies on the following aspects:aimed at specific subcellular structures, such as aspects of mitochondrial oxidative damage or cell terms of structures such as membrane protection. Therefore, the research these aspects of astaxanthin pharmacological activity and clinical application of a hot topic.We study the protection of astaxanthin on mitochondrial oxidative damage induced by ROS, the studies from the sub-cellular level and cell level.At the subcellular level,hydrogen peroxide (H2O2) is used to injury mitochondria extracte-d from rats liver; and investigate the protective effects of astaxanthin on mitochondria injury by ROS.The protective effects of astaxanthin on the oxidative injury of liver mitochondria were evaluated by the determination of GSH activity,complexⅠactivity,ATPase activity,mitochondria membrane permeability transition pore(PTP) open level were used Spectrophoto-meter.Mitochondria membrane fluidity was used Fluorescence spectrophotometer and mitochondria membrane potential was determine by Flow cytometry.At the cellular level,the oxidative injury of HepG-2 induced by H2O2, and investigate the protective effects of astaxanthin on mitochondria injury. The Cell viablity and inhibition ratio of mitochondria enzyme determined by MTT. Mitochondria membrane PTP open level was evaluated by Spectrophotometer. Mitochondria membrane potential and the content of ROS were evaluated by Confocal laser scanning microscope.Experimental results show:For the sub-cellular levels,the activity of GSH,complexⅠ,ATPase and mitochondria membrane potential were decreased obviously by H2O2;and p andηwere increased markedly by H2O2,mitochondria membrane fluidity decreased promptly (P<0.01),mitochondria membrane PTP was increased comparing to control group.While, astaxanthin (1.0×10-5,1.0×10-6mol·L-1), the activity GSH,complexⅠ,ATPase,mitochondria membrane fluidity and mitochondria membrane potential were increased obvious-ly(P<0.01,P<0.05); mitochondria membrane PTP open level was decreased markedly (P<0.01, P<0.05).From these result, it can be concluded that astaxanthin is beneficial in protecting rats liver mitochondria against oxidative damage induced by ROS with a dose-dependent,inhibition of mitochondrial membrane structure and energy metabolism in injury. For the cellular levels, the cell viablity and mitochondria membrane potential was decreased obviously comparing to control group;inhibition ratio of mitochondria enzyme,mitochondria membrane PTP open level and the content of ROS increased markedly(P<0.01). But,astaxanthin (1.0×10-5,1.0×10-6mol·L-1), the Cell viablity and mitochondria membrane potential was increased obviously (P<0.01,P<0.05); inhibition ratio of mitochondria enzyme,mitochondria membrane PTP open level and the content of ROS decreased markedly (P<0.01,P<0.05). From these results, it can be concluded that astaxanthin is beneficial in protecting HepG-2 cells by protect mitochindria membrane and function, against oxidative damage induced by ROS.From the above,it can be concluded that the astaxanthin is beneficial in protecting mitoch-ondria and cells against oxidative injury induced by ROS, and its mechanism is releation with anti-oxidation.