Studies On Protective Effect Of Selenium Bridged Cyclodextrin In Oxidative Stress Injury Of Caenorhabditis Elegans

According to the free radical theory of aging, one of the main causes of aging iscomposed of biological molecular damage by reactive oxygen species ROS. Thismeans that any can reduce the ROS factor, are likely to delay aging. Oxidativemetabolism in organisms produce free radicals in small amounts, antioxidant systemin vivo metabolism balance to maintain the timely removal of free radicals. But insome of the damage accumulation under the influence of a large number of freeradicals induced in vivo, insufficient antioxidant protection mechanism in the cell, sothat the generation of active oxygen accumulation and toxic to cells, imbalanceresulting in oxidation and antioxidation, this state is called oxidative stress.Glutathione peroxidase (GPX) in organism, is one of the most important antioxidantenzymes, which can eliminate the hydrogen peroxide and lipid peroxide in the body,blocking the active oxygen free radical further injury to the body, is the active oxygenof important free radical scavenger in vivo, has obvious effect on the treatment andprevention of Keshan disease, cardiovascular disease, inflammation and cancer etc.After in vitro, selenium cyclodextrins can enhance glutathione peroxidase activity. Inthis paper, we using Caenorhabditis elegans as a model to study the seleniumsubstituted cyclodextrin to affect their life and oxidative stress resistance, seleniumsubstituted cyclodextrins are antioxidant enzymes glutathione peroxidase (GPX)enzyme mimics, scavenge ROS role. In our experiments, we first use of differentdoses of selenium cyclodextrin treatment nematode, the results showed that0.5mMand5mM selenium substituted cyclodextrins can be raised to different extentnematodes glutathione peroxidase activity, and showed a dose dependent. In addition,generation of cyclodextrin treatment nematode with selenium before oxidative stressinjury of juglone or H2O2, found that0.5mM selenium cyclodextrin for nematodeoxidative stress can play a role in the protection of the best. And in the thermal stressunder the condition of35℃, with0.5mM selenium substituted cyclodextrin treatmentmakes the nematode resistance increased by12%. However, in the absence of oxidative stress conditions, selenium substituted cyclodextrin can not prolong the lifeof the nematode, even in the best dosages of oxidation of life is also no effect, andafter selenium cyclodextrin cultured nematodes from hatching to development, theaverage number of eggs laid, athletic ability and the control group have no difference,thus also shows that the selenium cyclodextrin treatment for nematode harmful. Tostudy the mechanism of selenium substituted cyclodextrin prolonged oxidation understress conditions of life, we have investigated the nematode lipid peroxidation andDNA damage level. The nematode is processed to juglone, the content of MDA willgreatly improve, nematodes and after0.5mM selenium substituted cyclodextrintreatment, MDA content decreased significantly, illustrate the ability of seleniumcyclodextrin has a strong inhibition of lipid peroxidation. On the other hand, oxidativestress can induce apoptosis, the DNA fracture, we using hydrogen peroxide tonematode for processing, the processed elegans DNA fragments electrophoresisanalysis, results show that hydrogen peroxide can be very obvious, due to thedissipation of DNA induced by DNA, broken, causing DNA damage; thus the use ofselenium substituted cyclodextrin treatment nematodes in hydrogen peroxidepretreatment, can effectively protect the nematodes from DNA damage caused byH2O2lock. In general, selenium substituted cyclodextrin can significantly resistoxidative stress, and to protect the nematodes from Hu Taokun and H2O2oxidativedamage, and thus further explains the important application of Selenium ofcyclodextrins in medical treatment.