In addition, no difference was seen on the cells viability when the cells were treated with genistein alone compared to controls.The scavenging ability on superoxide anion of homogenate from the IR group was weaker by compared to the sham group.The group subjected to IR had weaker hydroxyl scavenging ability than that of sham group about. The CA <a href="http://www.inhibit.online/archives/193">Targetmol's
cysteine</a> region of the hippocampus is susceptible to the transient ischemic insult.In the CA region from the IR group, the pyramidal cells have almost completely disappeared.There were cellsmm in the CAI region from the IR group, whereas there were cellsmm in the CA region from the sham group.In contrast to the IR group, pretreatment with CF signicantly increased the number of survival pyramidal cells in the CA region in a dosedependent fashion. The outcome of transient ischemic insult was also examined by transmission electron microscopy after ischemic insult for d.The nuclei of the pyramidal cells in the CA region from the sham group are normal; DNA evenly disperses in the nucleus, whereas most of the nucleus of the corresponding region from the IR group shrunk and the DNA condensed around the nucleus membrane.Some of the pyramidal cells of the CA region from the lowdose group suffered the same process as the IR group.The cells from the highdose group were similar to that of the sham group.The results suggests that pretreatment with CF protects the pyramidal cells in the CA region from IR damage.The reverse transcriptionpolymerase chain reaction products from total RNA of iNOS from the hippocampus were analyzed by electrophoresis with ethidium bromide in agarose gel.A single band was detected in RTPCR products from RNA of the iNOS.It was found that levels of mRNA in sham group are very weak, ischemiareprfusion enhanced the levels, and pretreatment with CF decreased the levels in hippocampus, suggesting that the enhancement of NO free radicals detected in the ischemiareperfusion might be generated by enhanced iNOS and the free radical decrease in the pretreated animal might come partly from the inhibition effect of CF on iNOS.It was found that the expression of NFB p was enhanced by about by ischemiareperfusion and pretreatment of CF decreased the expression in a dosedependent manner.There was a similar result for TNF; the enhancement of TNF reached about and pretreatment by CF signicantly decreased the expression of TNF especially for the higherdose group.This review suggests that some natural antioxidants can prevent neurodegenration, which might open a new way to protect against oxidativestressrelated disease.It is easy to take the natural antioxidants from drinking tea and soybean milk and eating fresh fruits and vegetables every day.Neuroreport. Toxicology. Toxicology. Toxicology. Biofactors. Korea Soybean Digest. Phytomedicine. J. NeuroChem. Molecular Neurobiology Volume, HUGHES, BSC NICOLETTA DOZIO, PHD DAVID A.Once shortened to a critical length, cells are triggered into replicative senescence.Type diabetes is associated with oxidative DNA damage, and we hypothesized that telomere shortening would characterize type diabetes.There was a trend toward increased oxidative DNA damage in all diabetes cell types examined and a signicant inverse relationship between oxidative DNA damage and telomere length in the diabetic group.