Levels Of Oxygen Free Radicals Research Articles

Chlorogenic acid prevents isoproterenol-induced DNA damage in vascular smooth muscle cells.

Numerous clinical therapeutic agents have been identified as DNA damaging. The present study revealed that isoproterenol (Iso) resulted in DNA damage in vascular smooth muscle cells (VSMCs) and increased the levels of intracellular oxygen free radicals. Administration of chlorogenic acid (CGA) inhibited this effect. Pretreatment with CGA abrogated the increase in protein expression levels of γ-H2A histone family member X, phosphorylated ataxia telangiectasia mutated, phosphorylated Rad3-related protein, breast cancer 1 and C-terminal Src homologous kinase induced by Iso. In addition, the increase in levels of intracellular reactive oxygen species (ROS) induced by Iso was inhibited by CGA pretreatment in a dose-dependent manner. The results of the present study suggest that CGA may inhibit Iso-induced VSMC damage via the suppression of ROS generation. Therefore, CGA may be a novel agent for the treatment of vascular diseases.

Genetic polymorphism of antioxidant enzymes in eosinophilic and non-eosinophilic nasal polyposis.

Chronic rhinosinusitis with nasal polyps (CRSwNP) is a chronic inflammatory disease of the paranasal sinuses, and its pathophysiology is not yet precisely known. It is suggested that oxygen free radicals play an important role in the pathogenesis of nasal polyposis. This study aimed to identify genetic polymorphisms of superoxide dismutase (SOD 2), catalase (CAT), and inducible nitric oxide synthase (iNOS) enzymes in eosinophilic CRSwNP and non-eosinophilic CRSwNP patients; the study also aimed to evaluate the effect of genetic polymorphism of antioxidant enzymes on CRSwNP etiopathogenesis. One hundred thirty patients, who received endoscopic sinus surgery due to CRSwNP, and 188 control individuals were included in this study. Nasal polyp tissues were divided into two groups histopathologically as eosinophilic CRSwNP and non-eosinophilic CRSwNP. Venous blood samples were taken from the patient and control groups. Polymorphisms in the Ala16Va1 gene, which is the most common variation of SOD-2 gene, and 21 A/T polymorphisms in catalase gene were evaluated with the restriction fragment length polymorphism method and -277 C/T polymorphism in the iNOS gene was evaluated with the DNA sequencing method. The GG genotype distribution for the (-277) A/G polymorphism in the iNOS gene was a statistically significant difference between eosinophilic CRSwNP and control groups (p<0.05). The CC genotype distribution for the SOD2 A16V (C/T) polymorphism was not statistically significant in all groups (p>0.05). The TT genotype distribution for the A/T polymorphism in catalase gene at position -21 was statistically significant differences in eosinophilic CRSwNP and control groups (p<0.05). Increased free oxygen radical levels, which are considered effective factors in the pathogenesis of CRSwNP, can occur due to genetic polymorphism of enzymes in the antioxidant system and genetic polymorphism of antioxidant enzymes in eosinophilic CRSwNP patients might contribute to the pathophysiology.

Current Literature Review.

Current Literature Review.

Normobaric oxygen paradox and erythropoietin production in critically ill patients: a prospective observational study

The normobaric oxygen paradox (NOP) postulates that a period of normobaric hyperoxia followed by a rapid return to normoxia will create a condition of relative hypoxia, which acts in turn as a stimulus for erythropoietin (EPO) production [1]. Variations in GSH and oxygen free radical (ROS) levels may be involved in this process. We tested the NOP in critically ill patients.

The Effects of Soybean Trypsin Inhibitor on Free Radicals Levels in Pancreatic Mitochondria of Mice

This paper aims to explore the effect of soybean trypsin inhibitor（STI） on oxygen free radicals levels in pancreatic mitochondria of mice. 36 male KM mice were randomly divided into three groups and fed with different diets as follows: control group was fed on control diet, STI group was fed on control diet containing STI, and VC (vitamin C) group was fed on STI diet supplemented with vitamin C. Mice were sacrificed by decapitation after being fed for 3 weeks. Pancreas was quickly removed and mitochondria were prepared for determining the oxidative and antioxidative index. The results showed that, compared with mice fed with control diet, malondialdehyde (MDA) content and activity of nitric oxide synthase (NOS) in pancreatic mitochondria of mice fed with STI diet were significantly increased (<i>P</i><i> </i>< 0.05), the content of glutathione (GSH), total antioxidant capacity (T-AOC), the activities of glutathione peroxidase (GSH-Px), catalase(CAT) and superoxide dismutase (SOD) were significantly dropped. After STI diet was supplemented with antioxidant, the contents of oxidation parameters were significantly decreased (<i>P</i><i> </i>< 0.05), but their values were still higher than those of control group; the activities of antioxidant parameters in pancreatic mitochondria were significantly increased (<i>P </i>< 0.05), but still lower than those of control group. These results supported that STI could cause oxidative stress in pancreatic mitochondria. In addition, vitamin C could interfere with the role of STI on the organism and effectively improve the status of oxidative stress.

Zinc supplement modulates oxidative stress and antioxidant values in rats with severe acute pancreatitis.

Oxidative stress is a main factor in the pathogenesis of severe acute pancreatitis (SAP). The ability of zinc (Zn) to retard oxidative processes has been recognized for many years. This study aims to examine the levels of free oxygen radicals and antioxidant enzyme in SAP rats and know the effect of Zn supplementation on free oxygen radicals and antioxidant system in rats with SAP. Forty-five male Wistar rats were divided into three groups-the SAP group (n=15), the Zn-treated group (n=15), and the controlled group (n=15). For the SAP group, sodium taurocholate is injected into the pancreatic duct to induce SAP; for the Zn-treated group, Zn (5 mg/kg) is subcutaneously injected immediately after injection of 5% sodium taurocholate. Firstly, the activity of erythrocyte glutathione peroxidase (GSH-Px), erythrocyte superoxide dismutase (SOD), and the content of plasma malondialdehyde (MDA), which are the toxic products of oxidative stress, is measured. Secondly, the levels of free oxygen radicals in the liver and kidney are detected. The result showed that the activity of GSH-Px and SOD was lower in the SAP group than that in the controlled group, although the content of plasma MDA increased. However, the activity of SOD and GSH-Px in the Zn-treated group was not significantly decreased after comparing with the controlled group; in the mean time, the content of MDA was not significantly increased either. Moreover, the content of free radical in liver and kidney was higher in the SAP group compared with the controlled group, but the content of free radical in the Zn-treated group was not higher than that in the controlled group (p>0.05). All of the above indicated that Zn may recover the activity of free radical-scavenging enzymes and decrease the content of free radical for the SAP group rats. In conclusion, the content of free radical increase may be one of the reasons that SAP rats are injured, and it is possible for Zn to be used to treat SAP through scavenging free radical and increasing the activity of SOD and GSH-Px of erythrocyte.

Increased adhesion formation after gelatin-thrombin matrix application in a rat model.

To evaluate the effects of gelatin matrix and thrombin-based hemostatic sealant agents (gelatin-thrombin matrix) on postoperative adhesion formation in the rat uterine horn model. A total of fourteen female Wistar-Albino rats were used in our postoperative adhesion formation model. Both uterine horns were exposed by midline incision with sterile technique and each uterine horn was traumatized by bipolar electrocautery. Before closure of the abdomen, 0.9% NaCl solution was administered intraperitoneally in the control group and the gelatin-thrombin matrix was applied on the traumatized areas on the uterine horns of the rats in the study group. At day 21 after the first surgery, the intraperitoneal macroscopic adhesion scores and the extent of fibrosis, inflammation scores, inflammatory cell activities, inflammation types of adhesion tissues, and the level of free oxygen radicals [malondialdehyde (MDA)] and antioxidant enzyme activity [superoxide dismutase (SOD) and glutathione S-transferase (GST)] in the uterine horn tissue were measured. There was no statistically significant difference between the two groups in terms of macroscopic adhesion scores (p=0.064), MDA levels (p=0.121), and GST activity (p=0.360). However, there was statistically significant difference between the two groups in terms of the extent of fibrosis (p<0.001), inflammation score (p=0.001), inflammatory cell activity (p=0.002), and SOD activity (p<0.001). Gelatin-thrombin matrix was found to have increased the extent of fibrosis, inflammatory cell activity, and inflammation score, and reduced the activity of SOD, which acts to prevent cell damage.

Picroside II Diminishes Oxidative Stress Induced By Cerebral Ischemic Injury In Rats

Stoke is a major health problem and there is no effective treatment of the disease. Therefore, finding novel chemicals that can be used to treat stroke has been an intensive research area. Picroside II seems to be a promising compound, yet its utilization in particular, the dosage and time window of its application after stroke has not been optimized. In this study, we wanted to address this problem using Malondialdehyde (MDA) and superoxide dismutase (SOD) as two parameters. MDA, a lipid peroxidation product formed by reactions between free radicals and polyunsaturated fatty acids, can be measured to reflect the magnitude of oxidative stress [1]. The aldehyde of MDA can occur crosslinking reaction with the amino groups of phosphatidylserine in neuronal membrane phospholipids [2]. The lipid peroxidation of biomembrane and its lipid peroxide products can also implicate the protein in the membrane to result in oxidative damage and apoptosis[3,4]. The content of MDA can reflect the levels of the free radicals and lipid peroxidation in tissue [5,6]. When the level of oxygen free radicals (OFR) elevates, SOD can react with superoxide anion with the generation of hydrogen peroxide. And hydrogen peroxide (H2O2) can turn into water under the effect of catalase and glutathione peroxidase to remove the OFR to protect cells from damage. Therefore, the level of SOD activity can reflect the ability of the body in clearing OFR [7,8]. Cell culture experiments confirmed that picroside II can reduce H2O2-induced injury in PC12 cells and improve cell survival [9,10,11]. Animal experiments showed that picroside II, an active ingredient of traditional Chinese medicine, can also inhibit the expression of inflammatory factors and apoptosis in cerebral ischemic penumbra, thus improve the neurobehavioral functions in rats [12,13,14]. Our group dealt the rats with different doses of picroside II at different ischemic time, and the result showed that the optimized therapeutic dose and time window of picroside II in cerebral ischemia reperfusion injury was ischemia 1.5 h with 20mg/kg body weight by intraperitoneal injection [15]. This study was designed to detect the MDA levels and SOD activity in blood and brain tissue to further explore the anti-oxidation effect and the optimal therapeutic dose and time window of picroside II in cerebral ischemic injury. Abstract

Protection by Atorvastatin Pretreatment in Patients Undergoing Primary Percutaneous Coronary Intervention Is Associated With the Lower Levels Of Oxygen Free Radicals

The aims of this study were to investigate the effects of atorvastatin pretreatment on the oxygen free radicals and its protective role on the myocardial cell during the ischemic reperfusion injury. One hundred fifty-six patients with ST elevation myocardial infarction undergoing percutaneous coronary interventions, aged from 29 to 85 years, were selected. Eighty patients were randomly assigned to placebo group and 76 to statin treatment (80-mg loading dose given a mean of 1.5 hours before percutaneous coronary intervention). The nitrogen monoxidum, malondialdehyde, and superoxide dismutase (SOD) were assayed before and after reperfusion. Thrombolysis in myocardial infarction (TIMI) grade and corrected TIMI frame count were measured after reperfusion. The creatine kinase-MB and troponin T peak levels after myocardial infarction were recorded. There was no significant difference in the nitrogen monoxidum, malondialdehyde, and SOD levels (P > 0.05) between the 2 groups before intervention. After the reperfusion, significantly lower creatine kinase-MB (289.9 ± 180.8 U/L vs. 360.5 ± 206.4 U/L, P = 0.025) and troponin T (4.60 ± 3.13 ng/mL vs. 6.01 ± 4.98 ng/mL, P = 0.035) peak levels can be observed in the statin versus the placebo group, and the SOD level of the statin group is higher than that of the placebo group (34.14 ± 15.07 U/mL vs. 29.06 ± 12.76 U/mL, P = 0.024). Atorvastatin can reduce oxygen free radicals developed in reperfusion, imposing protective effect on the myocardial cell during ischemic reperfusion injury.

Role of oxygen free radicals in the proliferation of myofibroblasts induced by AngII

Previous studies have demonstrated the important role of angiotension II (AngII) in promoting proliferation of myofibroblasts (myoFbs) and myocardial fibrosis. However, the underlying mechanisms and the role of oxygen free radicals in the proliferation of myofibroblasts induced by AngII are unclear. The present study was designed to shed light on this issue through exploration of AngII signaling pathways via in vitro experiments. Primary cultures of neonatal rat myoFbs were divided into five groups which were treated with AngII (10−8 to 10−6M), AngII with the antioxidant N-acetyl-L-cysteine (NAC), or normal culture medium. We observed the proliferation of myoFbs as induced by AngII at different concentrations with MTT. Reactive oxygen species (ROS) levels in myoFbs were detected by monitoring the fluorescence of 2′,7′-dichlorofluorescein. The contents and levels of oxygen free radicals (OH) in the three groups were detected by spectrophotometer, immunocytochemical staining, and confocal fluorescence. Western blot and image analysis were used to measure membrane translocation and expression of phospho-protein kinase Cα. MyoFbs incubated with AngII (10−8 to 10−6M) for 24h increased their rate of proliferation, the content of OH, and expression of ROS (P<0.01 vs. control group), whereas these parameters decreased in the presence of NAC. Immunocytochemistry, confocal fluorescence staining and image analysis showed that AngII could promote the translocation and expression of p-PKCα in membrane, and the antioxidant NAC blocked this increase (P<0.01). Western blot results also showed that NAC could inhibit the expression of p-PKCα.

The Association between Oxidative Stress and Metabolic Syndrome in Adults

BackgroundIn this Study, we investigated the effects of lifestyle and metabolic syndrome on free oxygen radical levels in men and women in Korea.MethodsA total of 254 adults were included in this study from February 2011 to June 2012 at a health promotion center. Information of the lifestyles and presence of metabolic syndrome factors was obtained. Biochemical markers were measured and free oxygen radicals test (FORT) was performed on the blood.ResultsOf the 254 subjects, 86 (33.9%) had metabolic syndrome, and 187 (73.6%) were men. Between the subjects with and without metabolic syndrome, there was a significant increase in alanine aminotransferase and serum FORT values in the subjects with metabolic syndrome. Multiple linear regression analysis showed that high-sensitivity C-reactive protein (hs-CRP) (P = 0.004), metabolic syndrome (P = 0.037), and female gender (P = 0.030) were independent predictors of serum FORT values. The subjects with high fasting blood sugar level or low high density lipoprotein cholesterol levels showed high serum FORT values.ConclusionHigh hs-CRP, the presence of metabolic syndrome, and female gender were associated with the high oxidative stress. High oxidative stress was associated with the presence of metabolic syndrome.

The protective effect of Ginkgo biloba extract against experimental cisplatin ototoxicity: animal research using distortion product otoacoustic emissions

Cisplatin, an effective therapeutic agent for various human cancers, has dose-limiting side effects of ototoxicity and nephrotoxicity. Cisplatin ototoxicity is thought to result from increased amounts of toxic free radicals or cell membrane changes leading to increased intracellular calcium content. Ginkgo biloba extract prevents lipid peroxidation, decreases intracellular free oxygen radical levels, regulates the cell membrane calcium transport mechanism and prevents cell death. This study aimed to investigate the protective effect of Ginkgo biloba extract against cisplatin-induced ototoxicity in rats. Twenty Wistar albino rats with normal hearing (confirmed by distortion product otoacoustic emission testing prior to cisplatin application) were randomly allocated to two groups. Both groups received a single intraperitoneal dose of cisplatin (12 mg/kg). Group two also received daily intraperitoneal doses of Ginkgo biloba extract (100 mg/kg) for 10 days. Distortion product otoacoustic emission measurements were repeated on days 10 and 17 and signal-to-noise ratios were compared. Compared with group one, group two had significantly better distortion product otoacoustic emission results at 3, 4, 6 and 8 kHz on days 10 and 17. These findings suggest that Ginkgo biloba extract protects the inner ear against cisplatin-induced ototoxicity.

Effects of subcutaneous and intraperitoneal administration of insulin to KK mice's oxygen free radicals metaholism

Objective To observe the subcutaneous and intraperitoneal insulin injection's effect of the level of oxygen free radicals of type 2 diabetes model.Methods C57BL/6J mice were chosen as normal control group (C group,n=9).KK mice were randomly divided into intraperitoneal injection of insulin group (i.p.group,n=9),the subcutaneous insulin group (s.c.group,n=9) and untreated group (U group,n =9).The i.p.group and the s.c.groups were given certain amount of insulin (insulin injecta and protamine insulin injecta by volume ratio of 2:1 mixture)for one month,maintained the GLU at normal levels (6±1.5) mmol/L.SOD,GSH-PX activity and MDA content of serum,liver,kidney and heart in each group were detected.Results The liver,kidney,heart and serum's SOD and GSH-PX activity significantly reduced and MDA content significantly increased in the U group.Both kinds of delivery methods could increase serum SOD and GSH-PX activity and reduce the content of MDA to the normal control group level,but the intraperitoneal injection had stronger effect.Two kinds of delivery methods could both reduce the MDA content of liver,and had almost the same effect; but the subcutaneous injection group had better effect on increasing the liver's SOD activity,and the intraperitoneal injection had better effect on increasing liver's GSH-PX activity.Intraperitoneal injection had better effect on reducing kidney' s MDA content and increased SOD activity.Two kinds of delivery methods had the same effect on reducing the heart's MDA content.Conclusion The two delivery methods can both make the MDA levels of KK mice in serum,heart,liver and kidney fall to as normal as that of control group,but the two delivery methods have different ways of improving the antioxidant capacity in different organs.Intraperitoneal injection can reduce MDA content in serum and kidney better. Key words: Diabetes; Insulin; Oxygen free radicals

Koroziv Özofajitin Geç Komplikasyonları Biyokimyasal Yöntemlerle Öngörülebilir: Ön Rapor

Objective: High tissue levels of free oxygen radicals (FORs) have been reported in corrosive esophagitis (CE). The present study aimed to determine whether prediction of injury and late complications in CE is possible based on blood levels of FORs, Interleukin (IL)-6, Tumor necrosis factor (TNF)-?, and IL-10. Material and Methods: Forty-two male Wistar albino rats were randomly divided into 2 main groups (A and B), each consisting of 3 subgroups (A1, A2, A3, B1, B2, and B3) of equal number. To induce experimental CE 17.5% NaOH was used in subgroups A2 and B2, and 37.5% NaOH in subgroups A3 and B3. The sham groups (A1 and B1) received 0.9% NaCl. Blood levels of lipid hydroperoxide (LPO) and glutathione peroxidase (GPx) were measured in group A. Blood levels of IL-6, IL-10, and TNF-? were measured in group B. Esophageal samples for histopathological evaluation were obtained following scarification after 3 weeks. Results: There were significant differences between the sham subgroups and CE subgroups, regarding histopathological scores (p< 0.05). There was no significant difference between the groups in blood levels of LPO, GPX, TNF-? or IL-10 (p> 0.05). There were significant differences between severe CE subgroups and the sham subgroups, based on IL-6 values (p= 0,007). Conclusion: In contrast to previous reports, which demonstrated increased tissue levels of FORs, blood levels of FORs were not high in this study. Nonetheless, in the light of the observed differences in IL-6 levels between the subgroups, we suggest that injury and late complications of CE may be predicted following additional experimental and clinical research using biochemical methods.

Assessment of Lifestyle Effects on the Levels of Free Oxygen Radicals in the Korean Population

BackgroundAs many studies revealed that oxidative stress due to the imbalance of reactive oxygen species (ROS) and antioxidant capacity is related with pathologic processes such as cardiovascular diseases, diabetes, as well as aging and obesity, the relationship between lifestyle and oxidative stress has recently gained much medical attention. However, little information exists on the effects of lifestyle on ROS in Korea. In this study, we investigated the effects of lifestyle on free oxygen radical levels in men and women in Korea.MethodsA total of 138 adults participated in this study from September 2007 to June 2010 at a health promotion center and department of family medicine. Information on the lifestyle of each participant was obtained by questionnaire. Biochemical markers and a free oxygen radical test (FORT) were also measured.ResultsThe average age was 47.28 ± 10.85 years and 79.7% were male. High sensitivity C-reactive protein (hs-CRP; r = 0.418, P = 0.012), triglycerides (r = -0.243, P = 0.008), hemoglobin (r = -0.445, P < 0.001), total protein (r = 0.210, P = 0.036), creatinine (r = -0.294, P = 0.001), fruit intake per day (P = 0.047), and smoking (P = 0.003) were related to the FORT levels in univariate analysis. Multiple linear regression analysis showed that hs-CRP (P = 0.039) was an independent predictor of serum FORT values. This statistical model can explain 78% of the variance in FORT values.ConclusionThis result suggests that hs-CRP showed a statistically significant positive association with FORT values. Further studies on the relationship between lifestyle and antioxidant capacity as well as ROS seem to be warranted to evaluate the overall effect of oxidative stress.

Relationship between Sonic hedgehog protein, brain-derived neurotrophic factor and oxidative stress in autism spectrum disorders.

The etiology of autism spectrum disorders (ASD) is not well known but oxidative stress has been suggested to play a pathological role. We report here that the serum levels of Sonic hedgehog (SHH) protein and brain-derived neurotrophic factor (BDNF) might be linked to oxidative stress in ASD. By using the whole blood or polymorphonuclear leukocytes, we demonstrated that autistic children produced a significantly higher level of oxygen free radicals (OFR). In addition, we found significantly higher levels of serum SHH protein in children with mild as well as severe form of autism. We also found that the serum level of BDNF was significantly reduced in autistic children with mild form of the disorder but not with severe form of the disorder. Our findings are the first to report a correlation between SHH, BDNF and OFR in autistic children, suggesting a pathological role of oxidative stress and SHH in autism spectrum disorders.

The influence of short-term l-arginine supplementation on rats’ muscular and hepatic cells in ischemia–reperfusion syndrome

Due to the complex mechanisms of L-arginine activity, it is difficult to determine the clinical significance of supplementation with this amino acid. The objective of this study was to determine the influence of short-term supplementation with L-arginine in stress conditions, induced by ischemia-reperfusion syndrome, by assessing the damage to muscular and hepatic cells on the basis of creatine kinase (CK), alanine aminotransferase (ALAT) and aspartic aminotransferase (AspAT) activity in blood and the level of oxygen free radicals in analyzed tissues of rats. We observed that induced ischemia of hind limb caused an increase in CK, ALAT and AspAT activity and an increase in the level of free radicals in liver, but not in skeletal muscle. Supplementation with L-arginine led to a reduction in serum activity of CK and AspAT and reduction of the level of free radicals in analysed tissues. Simultaneous supplementation with L -arginine AND L-NAME resulted in a reversal of changes induced by L-arginine supplementation in the case of AspAT and free radicals in skeletal muscle. The results indicate that under conditions of ischemia-reperfusion, short-term administration of L-arginine has a protective effect on skeletal muscle manifesting itself by reduction of CK in the serum and reduction of free radicals level in THIS tissue.

Gypenoside attenuates white matter lesions induced by chronic cerebral hypoperfusion in rats

Cerebral white matter lesions (WMLs) are frequently observed in vascular dementia and Alzheimer's disease and are believed to be responsible for cognitive dysfunction. The cerebral WMLs are most likely caused by chronic cerebral hypoperfusion and can be experimentally induced by permanent bilateral common carotid artery occlusion (BCCAO) in rats. Previous studies found the involvement of oxidative stress and astrocytic activation in the cerebral WMLs of BCCAO rats. Gypenoside (GP), a pure component extracted from the Gyrostemma pentaphyllum Makino, a widely reputed medicinal plants in China, has been reported to have some neuroprotective effects via anti-oxidative stress and anti-inflammatory mechanisms. In the present study, we investigated the protective effect of GP against cerebral WMLs and the underlying mechanisms for its inhibition of cognitive decline in BCCAO rats. Adult male Sprague–Dawley rats were orally administered daily doses of 200 and 400mg/kg GP for 33days after BCCAO, and spatial learning and memory were assessed using the Morris water maze. Following behavioral testing, oxygen free radical levels and antioxidative capability were measured biochemically. The levels of lipid peroxidation and oxidative DNA damage were also assessed by immunohistochemical staining for 4-hydroxynonenal and 8-hydroxy-2′-deoxyguanosine, respectively. Activated astrocytes were also assessed by immunohistochemical staining and Western blotting with GFAP antibodies. The morphological changes were stained with Klüver–Barrera. Rats receiving 400mg/kg GP per day performed significantly better in tests for spatial learning and memory than saline-treated rats. GP 400mg/kg per day were found to markedly scavenge oxygen free radicals, enhance antioxidant abilities, decrease lipid peroxide production and oxidative DNA damage, and inhibit the astrocytic activation in corpus callosum and optic tract in BCCAO rats. However, GP 200mg/kg per day had no significant effects. GP may have therapeutic potential for treating dementia induced by chronic cerebral hypoperfusion and further evaluation is warranted.

Genotoxic Effect of Chronic Exposure to DDT on Lymphocytes, Oral Mucosa and Breast Cells of Female Rats

The genotoxicity of some environmental contaminants may affect human health directly by damaging genetic material and thus plays an important role in cancer development. Xenoestrogens are one kind of environmental pollutants that may alter hormonal routes or directly affect DNA. The number of available biomarkers used to assess genetic risk and cancer is very extensive. The present study evaluated genotoxicity produced by the pesticide DDT on systemic and mammary gland cells obtained from adult female Wistar rats. Oral mucosa cells micronuclei were assessed; the comet assay in peripheral blood-isolated lymphocytes and mammary epithelial cells was also carried out. Additionally, oxidative stress was studied in mammary tissue through a lipid peroxidation assay. Our data showed an increase in lipid peroxidation, product of an increase in free oxygen radical levels, which leads to an oxidative stress status. Our results suggest that DDT is genotoxic, not only for lymphocytes but also to mammary epithelial cells.

Baicalein Significantly Protects Human Retinal Pigment Epithelium Cells Against H2O2-Induced Oxidative Stress by Scavenging Reactive Oxygen Species and Downregulating the Expression of Matrix Metalloproteinase-9 and Vascular Endothelial Growth Factor

Age-related macular degeneration is a leading cause of blindness in the elderly. At a later stage, neovascular or exudative age-related macular degeneration can lead to severe central vision loss that is related to aging-associated cumulative oxidative stress of the human retinal pigment epithelium (hRPE) cells. Early prevention with antioxidants is mandatory. The aim of this study was to determine whether and how baicalein can act as an antioxidant. The methods used included lactate dehydrogenase, 2′,7′-dichloro-fluorescein diacetate, or enzyme-linked immunosorbent assay to measure cell viability, oxygen free radical levels, or the levels of vascular endothelial growth factor (VEGF)/matrix metalloproteinase-9 (MMP-9), respectively. H₂O₂ dose-dependently reduced the cell viability of hRPE cells. This negative effect was dose-dependently (with a lower effect at 20µM) and significantly counteracted by pretreatment with baicalein (50µM). Treatment with H₂O₂ significantly stimulated the formation of oxygen free radicals. This increase was dose-dependently and significantly blunted by baicalein. Further, treatment with a sublethal dose of H₂O₂ was associated with an upregulation in the levels of VEGF and MMP-9. The increases in these proteins were also dose-dependently (with a lower effect at 20µM) and significantly (50µM) blunted by pretreatment with baicalein. This study supports an antioxidative role for baicalein whereby it protects hRPE cells against H₂O₂-induced oxidative stress by downregulating the levels of VEGF and MMP-9, which are increased by H₂O₂.