Tissue content of metalloproteinase-9 and collagen in the colon with and without fecal stream after intervention with infliximab in rats subjected to Hartmann's surgery

ABSTRACT Purpose Quantify the tissue content of metalloproteinase-9 (MMP-9) and collagen in colic mucosa with and without intestinal transit after infliximab administration in rats subjected to Hartmann's surgery. Methods Twenty-two rats underwent colon diversion by Hartmann's surgery. Animals were maintained with intestinal bypass for 12 weeks to induce development of diversion colitis (DC). Afterwards, animals were divided into three groups: first group received subcutaneous application of saline solution (SS) 0.9%, while the remaining two groups received infliximab subcutaneously at doses of 5 or 10 mg·kg-1·week-1 for five consecutive weeks. After the intervention, animals were sacrificed, removing the segments with and without intestinal transit. Diversion colitis was diagnosed by histological study, and its intensity was determined by a validated inflammatory scale. Tissue expression of MMP-9 was assessed byimmunohistochemistry, while total collagen was assessed by histochemistry. Tissue content of both was measuredby computerized morphometry. Results Colon segments without intestinal transit had a higher degree of inflammation, which improved in animals treated with infliximab. Collagen content was always lower in those without intestinal transit. There was an increase in the collagen content in the colon without transit in animals treated with infliximab, primarily at a dose of 10 mg·kg-1·week-1. There was an increase in the content of MMP-9 in the colon without fecal transit, and a reduction was observed in animals treated with infliximab, regardless of the dose used. Conclusions Application of infliximab reduces inflammation, increases the total collagen content and decreases the content of MMP-9 in the colon without intestinal transit.

Circulating levels of reactive oxygen species in patients with nonproliferative diabetic retinopathy and the influence of antioxidant supplementation: 6‑month follow‑up.

Aims: The aim was to evaluate circulating levels of reactive oxygen species (ROS) and changes in central macular thickness (CMT) in patients with nonproliferative diabetic retinopathy (NPDR) after antioxidant supplementation. Materials and Methods: A total of 68 patients (68 eyes) with NPDR were enrolled. Patients were randomly divided into two groups: Treated with antioxidant supplement (Group A) and untreated control group (Group B). Each tablet, for oral administration, containing pycnogenol 50 mg, Vitamin E 30 mg and coenzyme Q10 20 mg. CMT and free oxygen radical test (FORT) were analyzed at baseline (T0), 3 (T1) and 6 (T2) months in both groups. Results: In Group A, FORT levels and CMT were significantly reduced over time (P < 0.001 for both). In Group B, FORT levels were increased (P < 0.001) and CMT did not vary significantly (P = 0.81) over 3 time points. Conclusions: This is the first study showing the reduction of ROS levels in patients with NPDR thanks to antioxidant therapy. Moreover, our findings have suggested also an influence on retinal thickness.

Protective effect of trigonelline on rat cardiomyocytes during hypoxia and reoxygenation / 重庆医学

Objective To investigate the protective effects of trigonelline in neonatal rat cardiomyocytes during hypoxia /reoxygenation and its mechanism .Methods The neonatal rat cardiomyocytes was randomly divided into the normal control group , the hypoxia/reoxygenation group and the trigonelline group .Flow cytometry was used to determine the apoptosis and mitochondrial membrane potential .The levels of SOD and MDA were measured in different groups .Western blot method was used to measure the procaspase‐9 ,cleaved caspase‐9 ,procaspase‐3 and cleaved caspase‐3 protein level .Results Trigonelline could inhibit apoptosis (P<0 .05) ,enhanced activity of SOD (P<0 .05) ,reduce production of MDA (P<0 .05) ,stabilize the mitochondrial membrane potential (P<0 .05) and activate caspase‐9 and caspase‐3 in neonatal rat cardiomyocytes during hypoxia/reoxygenation .Conclusion Trigo‐nelline could protect myocardial cells from injury caused by hypoxia and reoxygenation ,and the mechanism may be associated with anti‐lipid peroxidation and stabilizing mitochondria membrane potential .

Oxidative stress and apoptosis in gut barrier dysfunction of severe acute pancreatitis / 中华急诊医学杂志

Objective By means of animal study,investigated the gut barrier function in severe acute pancreatitis ( SAP),and role of inflammatory factors releasing,gut mucosa oxidative stress,cell apoptosis in it.Methods The animal experiment was done in the animal center of first people' s hospital,shanghai jiaotong university.Twenty four BALB/c mice were randomized ( random number) divided into two groups with twelve mice each group.The SAP group,mice received six intraperitoneal injections of cerulein at 1-hour intervals, the dose was 50μg/kg, then given one intraperitoneal injection of 10 mg/kg lipopolysaccharide ( LPS from E.Coli) for the induction of severe acute pancreatitis.The control ( sham operation) group,the mice received intraperitoneal injection of 2 ml normal saline for six times at 1-hour intervals.All the animals of each group were averaged to two batches,4 h and 8h after being operated respectively,to be anesthetized and adopted blood and tissue specimen.Then we observed the pathological change of pancreas and gut,scored it.We measured the blood value of diamine oxidase ( DAO),amylase and tumor necrosis factor-α (TNF-α).We detected content of malondialdehyde (MDA),superoxide dismutase (SOD),glutathione (GSH) and activity of xanthine oxidase (XO) in gut mucosa.We detected the casepase-3 activity and cell apopotosis by means of terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) in gut mucosa,and conculated the apopotosis index (AI).Then using the PASW 18.0 software,we analyzed the data by anova and t-test,to make sure if the values were statistically different between the two groups and the mechanism of gut barrier dysfunction in panreatitis.Results At 4 h and 8 h after operation,the SAP-group-mice had significantly higher pancreas pathological score (P ＜0.01 ),blood amylase value ( P ＜ 0.05 ),gut pathological score and blood DAO and TNF-α value ( P ＜0.01 ),compared with the contral-group-mice.The gut mucosa MDA content and XO activity of mice in SAP group were significantly higher than which in control group ( P ＜ 0.01 ). The SAP-group-mice had significantly lower gut mucosa SOD content ( P ＜ 0.01 ) and GSH content ( P ＜ 0.05 ),compared with the contral-group-mice.The gut mucosa cells of mice in SAP group had significantly higher caspase-3 activity and apoptosis index than which in control group ( P ＜ 0.01 ).Conclusions In severe acute pancreatitis,inflammatory factors such as TNF-αwere waterfall-style released,induced gut mucosa suffer from ischemia-reperfusion injury,then serious oxidative stress developed in mucosa and activated caspase-3 pathway,inducing gut mucosa cells apoptose seriously,which was an important mechanism of gut barrier dysfunction.

Study on oxidative lipid and DNA damages in the malignant transformed BEP2D cells induced by α-particle exposure / 中华放射医学与防护杂志

Objective To investigate the mechanism of malignant transformation in human bronchial epithelial cell line BEP2D exposed to α-particles.Methods The levels of intracellular ROS and malonaldehyde (MDA) in BEP2D,RH22 (passage 22 of α-particle-irradiated BEP2D cells) and BERP35T-1 cells (derived from nude mice bearing malignant transformed cells generated from the passage 35 of α-particle-irradiated BEP2D cells) were assayed with DCFH-DA and MDA kit,respectively.The expressions of 8-OH-dG and γ-H2AX in BEP2D,RH23 (passage 23 of α-particle-irradiated BEP2D cells)and BERP35T-1 cells were also measured with immunocytochemistry and immunofluorescence staining.Results Compared to BEP2D cells,the levels of ROS ( t =4.30 and 3.94,P ＜ 0.05 ) and MDA ( t =4.89 and 15.10,P ＜0.05) increased in RH22 and BERP35T-1 cells.The expressions of 8-OH-dG (t =3.80 and 2.92,P ＜ 0.05 ) and γ-H2AX ( t =7.61 and 12.67,P ＜ 0.05 ) in RH23 and BERP35T-1 cells were also higher than those in BEP2D cells.Conclusions Oxidative stress induces lipid peroxidation and DNA damage leading to genomic instability,which could contribute to cellular malignant transforming process in the human bronchial epithelial cell line BEP2D with α-particle exposure.

Reactive oxygen species inactivation improves pancreatic capillary blood flow in caerulein-induced pancreatitis in rats

PURPOSE: Reactive oxygen species (ROS) inactivation was studied to determine alterations in the pancreatic capillary blood flow (PCBF) during caerulein-induced pancreatitis in rats. METHODS: A laser-Doppler flowmeter to measure PCBF and N-t-Butyl-Phenylnitrone (PBN) compound to inactivate ROS were used. Forty rats were divided in groups: 1) control; 2) caerulein; 3) PBN; 4) caerulein+PBN. Serum biochemistry and histopathological analyses were performed. RESULTS: PCBF measured a mean of 109.08 ± 14.54%, 68.24 ± 10.47%, 102.18 ± 10.23% and 87.73 ± 18.72% in groups 1, 2, 3 and 4, respectively. PCBF in groups 2 and 4 decreased 31.75 ± 16.79% and 12.26 ± 15.24%, respectively. Serum amylase was 1323.70 ± 239.10 U/l, 2184.60 ± 700.46 U/l, 1379.80 ± 265.72 U/l and 1622.10 ± 314.60 U/l in groups 1, 2, 3 and 4, respectively. There was a significant difference in the PCBF and serum amylase when compared groups 2 and 4. Cytoplasmatic vacuolation was present in groups 2 and 4. Otherwise, no qualitative changes were seen. CONCLUSION: ROS inactivation improves PCBF and minimizes the serum amylase increase during caerulein-induced pancreatitis. ROS effect may be one of the leading causative events in this model of acute pancreatitis.

OBJETIVO: A inativação de radicais livres (RL) foi estudada para determinar as alterações do fluxo capilar pancreático (FCP) na pancreatite aguda induzida por ceruleína em ratos. MÉTODOS: Um laser-Doppler fluxímetro determinou o FCP e o composto N-t-Butyl-Phenylnitrone (PBN), para inativar os RL, foi utilizado. Quarenta ratos foram divididos em 4 grupos: 1) controle; 2)ceruleína; 3) PBN; 4)ceruleína+PBN. Dosagens bioquímicas e análise histopatológica foram realizadas. RESULTADOS: O FCP foi em média 109.08 ± 14.54%, 68.24 ± 10.47%, 102.18 ± 10.23% e 87.73 ± 18.72% nos grupos 1, 2, 3 and 4, respectivamente. O FCP nos grupos 2 e 4 diminuíram em média 31.75 ± 16.79% e 12.26 ± 15.24%, respectivamente. A média da amilase sérica foi de 1323,70 ± 239.10 U/l, 2184,60 ± 700,46 U/l, 1379,80 ± 265,72 U/l e 1622,10 ± 314,60 U/l nos grupos 1, 2, 3 e 4, respectivamente. Observou-se diferença significante no FCP e na amilase sérica quando comparados os grupos 2 e 4. Vacuolização citoplasmática estava presente nos grupos 3 e 4. Não foram observadas outras alterações qualitativas. CONCLUSÃO: A inativação de RL melhorou o FCP e minimizou a elevação da amilase sérica na pancreatite aguda induzida por ceruleína. A presença de RL parece ser um evento precoce neste modelo de pancreatite aguda experimental.

The Protective Effect of Free Oxygen Radical Inhibitors on Na-salicylate Induced Cochlear Damage in Guinea Pig / 대한이비인후과학회지

BACKGROUND AND OBJECTIVES: To elucidate the mechanism of salicylate ototoxicity of free oxygen radicals (FORs), we made an animal model with Na-salicylate cochlear toxicity and evaluated the protective effect of free oxygen radical inhibitors. MATERIALS AND METHODS: Na-salicylate soaked in gelfoam was placed on the round window niche of guinea pigs for 2 hours. After removal of gelfoam, electrocochleography and evoked otoacoustic emission test were performed at regular time intervals. These tests were repeated to see the protective effect of FORs inhibitors after the injection of allopurinol or superoxide dismutase (SOD). RESULTS: Hearing loss was noted after removal of gelfoam which was soaked with Na-salicylate. After 6 hours, these ototoxicity effects disappeared. The OAE test showed similar response. FORs inhibitors showed protective effects and SOD was more effective than allopurinol. CONCLUSION: These results support the idea that FORs activity contributes to ototoxicity of Na-salicylate. This damage can be diminished by treatment with drugs that scavenge and inhibit the formation of FORs.

Influence of tetramethylpyrazine on oxygen metabolism during the respi ratory burst of human neutrophiis / 中国临床药理学与治疗学

AimTo investigate the influence of tetramethylpyrazine(ligustrazine, Lig) on oxygen consumption and superoxide during the respiratory burst of human neutrophils. MethodsIt was observed by using ESR spin trapping, spin probe oxymetry and luminol-dependent chemiluminesence(CL) . Results Lig had no influence on oxygen consumption during the respiratory burst of neutrophils(P＞0.05), but had remarkable inhibition on CL response generated by neutrophils(P＜0.01), and had scavenging effect on O2 and OH ·generated by neutrophils, which were demonstrated in xanthine/ xanthine oxidase system and Fentons reaction(P＜0.01) . ConclusionLig has no inhibiting effect on oxygen metabolic function of neutrophils,but protects tissue from injury caused by activated neutrophils through scavenging oxygen radicals.

Influence of tetramethylpyrazine on oxygen metabolism during the respiratory burst of human neutrophils / 中国临床药理学与治疗学

0.05), but had remarkable inhibition on CL response generated by neutrophils(P

Effects of ST-1 against focal cerebral ischemia-reperfusion injury in rats / 中国临床药理学与治疗学

AIM: To demonstrate the protective effects of ST-1 against focal cerebral ischemia-reperfusion injury in rats.METHODS: The model of focal ischemia-reperfusion was induced by middle cerebral artery occlusion 2 h followed by reperfusion 22 h in rats.Neurological deficit scores were evaluated.Infarct size,malondialdehyde(MDA) content and superoxide dismutase (SOD) activity were measured,pathological changes of neurons in hippocampal CA1 region were observed.RESULTS: Compared with vehicle group ST1 at dose of 10 and 20(mg?kg~(-1)) could reduce the infarct size,MDA content,enhance SOD activity and relieve neurons injury in hippocampal CA1 region in dose-dependent way;ST-1 at dose of 20(mg?kg~(-1)) could also improve neurological function.CONCLUSION: ST-1 can protect brain tissue from focal ischemia-reperfusion injury.

Effects of small molecular antioxidants on cerulein-induced acute pancreatitis in rat

It has been suggested that oxygen free radicals are involved in the initiation process of acute pancreatitis, although its pathogenesis is not clear. This study evaluates the roles of oxygen radicals and the effects of small molecular antioxidants (rebamipide, N-acetyl-cysteine, allopurinol, beta-carotene) on the development of cerulein-induced acute pancreatitis. Acute edematous pancreatitis was induced by the intravenous infusion of cerulein at supramaximal dose of 10 mug/kg/hour for 3.5 hours. The effects of antioxidants, rebamipide (100 mg/kg, i.p.), N-acetyl-cysteine (200 mg/kg, i.v.), allopurinol (20 mg/kg/hour), beta-carotene (50 mg/kg, i.p.), were examined. Cerulein administration resulted in a significant increase in serum amylase activity and pancreatic malondialdehyde (MDA), but not glutathione peroxidase (GSHpx). The glutathione (GSH) content in pancreatic tissue decreased dramatically. Pretreatment of N-acetyl-cysteine significantly decreased the cerulein-induced hyperamylasemia and maintained GSH content in pancreas, but MDA was slightly decreased. In addition, N-acetyl-cysteine ameliorated histological damage. Allopurinol and beta-carotene attenuated cerulein-induced hyperamylasemia, but histologically there was no difference from control. These results indicate that oxygen free radicals play an important role in the initiation of experimental acute pancreatitis. N-acetyl-cysteine is an effective antioxidant that ameliorates the cerulein-induced acute pancreatitis, and the possible therapeutic application of antioxidants against acute pancreatitis needs a further evaluation.

Electrolysis of physiological salt solution generates a factor that relaxes vascular smooth muscle

Oxygen-derived free radicals have been implicated in many important functions in the biological system. Electrical field stimulation (EFS) causes arterial relaxation in animal models. We found that EFS applied to neither muscle nor nerve but to Krebs solution caused a relaxation of rat aorta that had been contracted with phenylephrine. In the present study, therefore, we investigated the characteristics of this EIRF (electrolysis-induced relaxing factor) using rat isolated aorta. Results indicated that EIRF acts irrespective of the presence of endothelium. EIRF shows positive Griess reaction and is diffusible and quite stable. EIRF-induced relaxation was stronger on PE-contracted aorta than on KCl-contracted one, and inhibited by the pretreatment with methylene blue. Zaprinast, a cGMP-specific phosphodiesterase inhibitor, potentiated the EIRF-induced relaxation. NG-nitro-L-arginine, NO synthase inhibitor, did not inhibit the EIRF-induced relaxation. Deferroxamine, but not ascorbic acid, DMSO potentiated the EIRF-induced relaxation. These results indicate that electrolysis of Krebs solution produces a factor that relaxes vascular smooth muscle via cGMP-mediated mechanism.

The effects of oxygen radicals on the activity of nitric oxide synthase and guanylate cyclase

Reactive oxygen species such as superoxides, hydrogen peroxide (H2O2) and hydroxyl radicals have been suggested to be involved in the catalytic action of nitric oxide synthase (NOS) to produce NO from L-arginine. An examination was conducted on the effects of oxygen radical scavengers and oxygen radical-generating systems on the activity of neuronal NOS and guanylate cyclase (GC) in rat brains and NOS from the activated murine macrophage cell line J774. Catalase and superoxide dismutase (SOD) showed no significant effects on NOS or GC activity. Nitroblue tetrazolium (NBT, known as a superoxide radical scavenger) and peroxidase (POD) inhibited NOS, but their inhibitory actions were removed by increasing the concentration of arginine or NADPH respectively, in the reaction mixture. NOS and NO-dependent GC were inactivated by ascorbate/FeSO4 (a metal-catalyzed oxidation system), 2'2'-azobis-amidinopropane (a peroxy radical producer), and xanthine/xanthine oxidase (a superoxide generating system). The effects of oxygen radicals or antioxidants on the two isoforms of NOS were almost similar. However, H2O2 activated GC in a dose-dependent manner from 100 microM to 1 mM without significant effects on NOS. H2O2-induced GC activation was blocked by catalase. These results suggested that oxygen radicals inhibited NOS and GC, but H2O2 could activate GC directly.

Antioxidant Effect of Allopurinol on Oxygen Radical-Induced Toxicity in Cultured Mouse Cerebral Neurons / 체질인류학회지

In order to elucidate the neurotoxic effect of oxygen radicals on cultured mouse cerebral neurons, the neurotoxicity induced by xanthine oxidase (XO) and hypoxanthine (HX), was evaluated by MTT assay. The neuroprotective effect of allopurinol against oxidant -mediated neurotoxicity was also examined in these cultures by MTT assay and neurofilament enzymeimmunoassay (EIA) with light microscopy. The results were as follows: 1. Oxygen radicals induced degenerative changs such as the decrease of cell number and the loss of neurites in cultured mouse cerebral neurons. 2. The value of midcytotoxicity value (MTT50) of oxygen radicals was estimated at a concentration of 20 mU/ml XO and 0.1 mM HX for 4 hours in these cultures. 3. Cell viability of cultured mouse cerebral neurons was significantly decreased by XO/HX in a dose -and time -dependent manners. 4. Allopurinol was very effective in blocking the neurotoxicity induced by XO/HX at a concentration of 30 microM as determined by MTT assay and neurofilament enzymeimmunoas-say. From the above results, it is suggested that oxygen radicals show neurotoxicity, and the selective antioxidant such as allopurinol are very effective in blocking oxidant -mediated neurotoxicity on cultured mouse cerebral neurons.

Effect of Glutathione on Oxidant-induced Cardiotoxicity

BACKGROUND: In order to elucidate toxic mechanism of the oxygen radicals on cultured rat myocardial cells, cytotoxic effect of oxygen radicals was evaluated by MTT assay. In addition protective effect of glutathione(GSH) on oxidant-induced cardiotoxicity was investigated on these cultures. METHODS: Myocardial cells derived from neonatal rats were cultured for 12 hours in the medium containing various concentrations of glucose oxidase(GO). Cell viability was measured by MTT assay and morphological changes of the myocardial cells were observed by light microscope. RESULTS: GO-mediated oxygen radicals remarkably decreased cell viability of cultured myocardial cells in a dose-and time-dependent manner. And also, GSH blicked GO-induced cardiotoxicity in these cultures. CONCLUSION: These results suggest that the oxygen radicals are tixic and the selective antioxidants such as GSH are effective in blocking against the oxidant-induced cardiotoxicity in cultures of the myocardial cells of neonatsl rats.

An Effect of Allopurinol on Salicylate Ototoxicity in Guinea Pigs / 대한이비인후과학회지

The mechanism of salicylate ototoxicity appears to be multifactorial and decreased cochlear blood flow seems to play an important role. The purpose of the study was to assess an effect of allpurinol, a blocker of free oxygen radicals(FORs) formation, on salicylate ototxicity in guinea pig. ABR threshold shifts were observed in group 1, treated with salicylate(300mg/kg, IM) and group 2, pretreated with allopurinol(50mg/kg, PO, two times) before injection of salicylate(300mg/kg, IM). In group 1, significant ABR threshold shift was measured in 1 hour(p<0.05) and maximum threshold shift was noted in 2-3 hours, with complete recovery in 6 hours, after injection of salicylate. In group 2, there was a little ABR threshold shift through 6 hours after injection of salicylate, except average 5dB shift in 4 hours. ABR threshold shift was significantly greater in group 1 than in group 2, after injection of salicylate(p<0.05). With above result, allopurinol, a blocker of FORs formation, could attenuated the hearing loss after the administration of salicylate in guinea pig, and FORs might play a role in salicylateinduced hearing loss.

The Effect of UVB Radiation on the Cultured Rabbit Lens Epithelial Cells

The present study has been conducted to assess the possible mechanism of cultured rabbit lens epithelial cell(LEC) damage and generation of oxygen free radicals after UVB exposure as well as to investigate the role of antioxidants to the survival rate of epithelial cells. Cultured rabbit LECs were exposed to various fluences of UVB radiation. The release of oxygen radicals(superoxide radical and hydrogen peroxide) and the activity of antioxidants(SOD, catalase) were also measured. The protective effects of various antioxidants on LECs damage after UVB exposure were measured. UVB radiation brought about a decrease in the survival fraction of cultured rabbit LECs. Exposure of the cells to fluences of 400 mJ/cm2, 1,600 mJ/cm2 and above 2,400 mJ/cm2 of UVB radiation resulted in 50%, 10%, nearly 0% in cell survival fraction, respectively. Cultured rabbit LECs exposed to UVB and hydrogen peroxide. The activity of intracellular SOD(esp. Cu, Zn-SOD) was significantly increased, but the activity of intracellular catalase was not changed. Antioxidants pretreatment(SOD, catalase, purpurogillin and allopurinol) ameliorated the cytoxoxic effect of UVB on the cultured rabbit LECs. These rusults indicate that the release of oxygen radicals are enhenced by exposure of LECs to UVB radiation. The oxygen radicals seem to play a specific role in the cytotoxic effect of LECs after UVB exposure.

Effect of Oxygen Radicals on Cultured Cerebral Neurons of Neonatal Mouse

PURPOSE: In order to elucidate the neurotoxic mechanism of oxygen radicals which are pathological factor of ischemia, we evaluated the oxidant-induced neurotoxicity and the neuroprotective effect of antioxidant on cultured cerebral neurons derived from neonatal mouse. METHODS: Neurotoxic effect was investigated after cultured mouse neuronal cells were exposed to oxygen radicals which were generated enzymatically by reaction of xanthine oxidase (XO) and hypoxanthine (HX). And also the neuroprotective effect of antioxidant was assessed with catalase. Both effects determined by cell viability were assessesd by MTT assay and neurofilament enzymeimmuno assay (EIA). In order to see the histologic change microscopic exam also done on the cerebral neuronal cells. RESULTS: 1) Oxygen radicals were toxic on cultured mouse cerebral neurons in dose- and time-dependent manner. 2) The value of lethal concentration50 (LC50) of oxygen radicals was estimated at a concentration of 25mU/ml xanthine oxidase (XO) and 0.2mM hypoxanthine (HX) in these culture. 3) Catalase was effective in blocking the neurotoxicity induced by oxygen radicals at a concentration of 50ug/ml. 4) Oxygen radicals induced the decrease of cell number and the loss of neurites in cultured mouse cerebral neurons. CONCLUSION: It is suggest that oxygen radicals cause the neurotoxicity and the selective antioxidants such as catalase are very effective in blocking oxidant-mediated neurotoxicity on cultured cerebral neurons of neonatal mouse.

Effect of Allopurinol on Methylmercuric Chloride in Cultured O1igodendrocytes / 체질인류학회지

To elucidate the neurotoxic mechanism of methylmercury on cultured bovine oligodendrocytes, neurotoxic effect was estimated by MTT assay after cultures were exposed to various concentrations of methylmercuric chloride (MMC). In addition, neuroprotective effect of antioxidant, allopurinol agonist MMC-induced neurotoxicity was examined on these cultures. Exposure of cultured bovine oligodendrocytes to MMC showed less than 50% of the cell viability 24 hours after treatment with 35µM of MMC. And also, allopurinol blocked the neurotoxicity induced by MMC on these cultures. These results suggest that oxygen radicals involve in MMC-mediated neurotoxicity, and also seletive antioxidants such as allopurinol are effective in blocking the neurotoxicity induced by MMC on cultured bovine oligodendrocytes.

Effects of Reactive Oxygen Species on Hyperactivation of Human Sperms / 대한비뇨기과학회지

capacitation of human sperm is essential for fertilization and is characterized visually by hyperactivated motility. There is a controversy whether reactive oxygen radicals cause infertility or stimulate sperm-zona interaction. We investigated the exact role of reactive oxygen radicals on hyperactivation (HA) of human sperm which could be a part of the capacitation process. Hyperactivation of human sperm was compared to the Ham's F-10 controls by the addition of superoxide anion and hydrogen peroxide generating enzymes on the percale treated sperms. The motility parameters of human sperms were estimated by computer assisted semen analysis system. The addition of xanthine + xanthine oxidase + catalase (generating system of superoxide anion and removal of hydrogen peroxide) on the sperms induced levels of HA (10.5% at 2 hour, 11.3% at 5 hour) which were about 2 times higher than those of controls (HA: 5.4% at 2 hour, 5.6% at 5 hour). The addition of glucose + glucose oxidase (generation of hydrogen peroxide) decreased the levels of HA (0.0% at 2 and 5 hour) significantly. Superoxide dismutase, the scavenger of superoxide anion inhibited HA significantly, whereas catalase, the scavenger of hydrogen peroxide promoted HA significantly These results suggest that the reactive oxygen radicals may be involved in hyperactivation of human sperms by the way that superoxide anion promotes and hydrogen peroxide inhibits hyperactivation of the fertile human sperms. It may be very important in the process of fertilization that promotion or inhibition of hyperactivation occurs at the proper time and location of female genital organ.