Combined application of Er:YAG and Nd:YAG lasers in treatment of chronic periodontitis. A split-mouth, single-blind, randomized controlled trial.

BACKGROUND: The aim of the present study was to compare the effectiveness of combined Er:YAG and Nd:YAG laser therapy to that of scaling and root planing with hand instruments in non-surgical treatment of chronic periodontitis. MATERIAL AND METHODS: Twenty-five systemically healthy patients with chronic periodontitis were selected for this study. The quadrants were randomly allocated in a split-mouth design to either combined Er:YAG (160 mJ/pulse, 10 Hz) and Nd:YAG laser (100 mJ/pulse, 20 Hz) therapy (test group) or scaling and root planing alone (control group). At baseline, 1 month and 3 months after treatment, plaque index, gingival index, probing depth, clinical attachment level and bleeding on probing (%), were recorded and gingival crevicular fluid and subgingival plaque samples were taken. The gingival crevicular fluid levels of interleukin-1ß and tumor necrosis factor-α were analyzed by enzyme-linked immunosorbent assay. Quantitative analysis of red complex bacteria was performed using quantitative real-time polymerase chain reaction. RESULTS: The clinical parameters had significantly improved for both groups after treatment. There were statistically significant differences in probing depth and clinical attachment level between the test and control groups only for deep pockets (≥7 mm) (P<.05). No significant differences between the two groups were observed for the biochemical and microbiological parameters at any time points (P>.05). CONCLUSIONS: The present study suggests that a combined course of Er:YAG and Nd:YAG laser therapy may be beneficial particularly in inaccessible areas such as deep pockets on a short-term basis. Further, well-designed studies are required to assess the effectiveness of the combination of these lasers.

Levels of interleukin-37 in gingival crevicular fluid, saliva, or plasma in periodontal disease.

BACKGROUND AND OBJECTIVE: The aim of this study was to compare the levels of levels of interleukin-37 (IL-37) in gingival crevicular fluid, saliva and plasma in patients with periodontal disease and patients with healthy periodontium and to correlate these levels with clinical parameters. MATERIAL AND METHODS: Samples of gingival crevicular fluid, whole saliva and plasma were collected from systemically healthy, nonsmoker periodontally healthy controls (group 1, n = 20), gingivitis patients (group 2, n = 20) and chronic periodontitis patients (group 3, n = 20). Full-mouth clinical periodontal parameters, including probing depth, plaque index, gingival index and bleeding on probing, were also recorded. IL-37 levels in the biofluid samples were determined by ELISA. Data were tested statistically using the Kruskal-Wallis test followed by the Mann-Whitney U-test. RESULTS: The concentration of IL-37 in gingival crevicular fluid was significantly lower in group 3 than in groups 1 and 2 (p = 0.001), whereas the total amounts in gingival crevicular fluid samples were similar (p > 0.05). The salivary and plasma concentrations of IL-37 were similar in the study groups (p > 0.05). There were negative correlations between gingival crevicular fluid IL-37 concentrations and gingival crevicular fluid volume in all groups (p < 0.05). There was also a negative correlation between the gingival crevicular fluid IL-37 concentration and gingival index in group 3 (p < 0.05). CONCLUSIONS: IL-37 was expressed in all biofluids. According to our findings, the total amount of IL-37 in gingival crevicular fluid, or salivary or plasma concentrations of IL-37, may not be useful diagnostic markers to differentiate periodontal disease and the periodontally healthy condition. The difference in gingival crevicular fluid IL-37 concentration between the study groups may be a result of the variation in gingival crevicular fluid volume, as suggested by the negative correlation between gingival crevicular fluid volume and gingival crevicular fluid IL-37 concentration. In the light of our findings, it seems that IL-37 is not involved in periodontal disease. Further comprehensive studies may clarify this issue more clearly.

Association of antepartum vitamin D levels with postpartum pelvic floor muscle strength and symptoms.

INTRODUCTION AND HYPOTHESIS: Vitamin D affects skeletal muscle strength and functions via various mechanisms. Strength and/or functional dysfunctions of the pelvic floor muscles may be associated with the distortion of pelvic floor functions. We hypothesized that vitamin D deficiency may contribute to pelvic floor dysfunction (PFD) by affecting pelvic floor muscle strength (PFMS). The aim of this study was to assess the effect of vitamin D deficiency during pregnancy on postpartum PFMS. METHODS: This cross-sectional study was conducted in a university hospital. One hundred and eighty pregnant women were admitted to our hospital in their third trimester and compared with 156 healthy nulliparous women. Venous blood samples for examining vitamin D levels were taken from each participant and stored at -80 °C. At 8-10 weeks postpartum, patients were invited to the hospital, asked about their PFD symptoms, and PFMS was measured using a perineometer. RESULTS: There was no statistical significance among groups regarding mean age, maternal age, and weight at delivery. Postpartum PFMS and duration in vitamin D-deficient women were significantly lower than those without the deficiency. Vitamin D-deficient vaginal delivery cases (group I) had a postpartum PFMS average of 21.96 ± 7.91 cm-H2O, nonvitamin D-deficient normal delivery cases (group III) had a PFMS of 29.66 ± 10.3 cm-H2O (p = 0.001). In the cesarean delivery groups, vitamin D-deficient (group II) and nonvitamin D-deficient (group IV) cases had PFMS values of 32.23 ± 9.66 and 35.53 ± 15.58 cm-H2O respectively (p = 0.258). CONCLUSIONS: Lower vitamin D levels in the third trimester correlates with decreased PFMS.

The role of prothrombotic factors in children with hemiplegic cerebral palsy.

AIM: Hemiplegic cerebral palsy (HCP) is a condition occurring as a consequence of a non-progressive damage of the brain with incomplete anatomical and physical development during the early period of life. Its etiology is multifactorial, with the cause remaining unexplained in the majority of cases. This study aims to investigate whether thrombophilic factors correlates with the etiology in children with HCP. METHODS: We included 36 children with HCP in the patient group, and 41 healthy children with no neurologic disorders in the control group. No significant difference was found between the two groups in terms of factor V leiden, methylenetetrahydrofolate reductase and prothrombin 20210A mutation frequency and protein C, protein S and antithrombin III levels. RESULTS: Homocysteine levels were significantly higher in the group of patients with HCP as compared to the control group (P=0.012). Because we could not identify the origin of hyperhomocysteinemia as congenital or acquired, the impact of hyperhomocysteinemia on HCP was considered insignificant. Each thrombophilic disorder was assessed in terms of relatedness to atrophy, periventricular leukomalacia, infarct, congenital anomaly and porencephalic cyst, respectively. No significant correlation was detected between thrombophilic disorders and cranial imaging findings. CONCLUSION: Our study has shown that thrombophilic factors are not involved in the etiology of HCP.

Genetic polymorphisms of paraoxonase1 192 and glutathione peroxidase1 197 enzymes in familial Mediterranean fever.

Familial Mediterranean fever (FMF) is an autosomal recessive disorder and is the most frequent of the periodic febrile inflammatory syndromes. The pathogenesis of the disease is not completely understood, even though the FMF gene has been identified. Oxidative stress and inflammation may play a role in the pathogenesis of FMF. We investigated gene polymorphisms of the antioxidative enzymes, glutathione peroxidase (GPX) and paraoxonase (PON) in FMF patients, and possible associations with FMF pathogenesis. Sixty FMF patients during an attack-free period and 51 healthy children as the control group were included in our study. PON1 Q/R192 and GPX1 Pro197Leu gene polymorphisms were assayed. Blood urea nitrogen, creatinine and serum lipid profile were also measured. PON1 Q/R192 genotype distribution was 52% QQ, 46% QR and 2% RR in the FMF group and 45% QQ, 45% QR and 10% RR in the control group (P>0.05). GPX1 Pro197Leu genotype distribution was 28% PP, 57% PL, 15% LL in the FMF group and 18% PP, 53% PL, 29% LL in the control group (P>0.05). Blood urea nitrogen, serum creatinine, lipid levels, and the distribution of PON1 Q/R192 and GPX1 Pro197Leu genotypes were similar in the two groups. We conclude that the PON1 Q/R192 and GPX1 Pro197Leu gene polymorphisms are not important risk factors in the development of FMF. However, larger studies are warranted to validate these conclusions.

The efficacy of minocycline against methotrexate-induced pulmonary fibrosis in mice.

OBJECTIVES: In addition to its antimicrobial effects, inhibitory effects of minocycline have been demonstrated, including against inflammation, apoptosis, proteolysis, angiogenesis, and tumor metastasis. In this study, we aimed to determine the beneficial effects of minocycline on lung histology and its antioxidant activity in a murine model of pulmonary fibrosis. MATERIALS AND METHODS: Twenty-eight Swiss albino mice were randomly allocated into four groups of seven animals per group. Group I (control group) received intraperitoneal injection of saline. Group II (methotrexate group) received methotrexate orally 3 mg/kg for 28 days. Group III (minocycline group) received methotrexate orally 3 mg/kg and 15 mg/kg of intraperitoneally injected minocycline for 28 days. Group IV (minocycline group) received 15 mg/kg of intraperitoneally injected minocycline for 28 days. Twenty-eight days later, the animals were euthanized. Thereafter, lung tissue samples were harvested. Histological findings of airways were evaluated by light microscopy. The levels of malondialdehyde (MDA), the product of reactive oxygen in lung tissue, and catalase, an antioxidant enzyme, were also determined. RESULTS: In the light microscopic examination, the lung tissues of the control group showed normal histological features. In the methotrexate group, the degree of lung damage (grade 3 fibrosis) was higher than the control and other groups (p: 0.001). In the minocycline-treated group, improvement in lung tissue was noted (median fibrosis score: 3 (MTX group) vs 1 (MTX plus minocycline group); p: 0.001). Only the minocycline group showed normal histological features. Although minocycline reduced the MDA levels in lung tissue, an increase in catalase activity was detected (p: 0.018 and p: 0.014, respectively). CONCLUSIONS: The administration of minocycline may be effective in MTX-induced lung fibrosis in mice. However, further studies with high-dose and long-term treatments are needed.

Proinflammatory cytokine levels in hyperlipidemic patients with periodontitis after periodontal treatment.

OBJECTIVE: The aim of this study was to evaluate the effects of periodontal treatment on serum and gingival crevicular fluid (GCF) proinflammatory cytokine levels in hyperlipidemic patients with periodontitis. MATERIALS AND METHODS: Fifty-two patients with hyperlipidemia and periodontitis and 28 systemically healthy controls with periodontitis (C) were included in the study. Hyperlipidemic groups were divided into two groups as suggested diet (HD) and prescribed statin (HS). The clinical periodontal parameters, fasting venous blood, and GCF samples were obtained, and serum tumor necrosis factor-alpha (TNF-α), interleukin (IL) 1-beta, and IL-6 levels were evaluated at baseline and at 3 months follow-up (3MFU) after the completion of the non-surgical periodontal treatment that included scaling and root planning. RESULTS: Percentage of bleeding on probing was significantly higher in the HS group than both the HD and C groups. In the HD and HS groups, there were significant decreases in serum IL-6 and GCF TNF-α levels between the 3MFU and baseline. A significant decrease was also found in GCF IL-6 at the end of the study period in the HS group. CONCLUSION: The combination of the periodontal therapy and antilipemic treatment may provide beneficial effects on the metabolic and inflammatory control of hyperlipidemia.

The impact of the IL-11:IL-17 ratio on the chronic periodontitis pathogenesis: a preliminary report.

OBJECTIVE: An imbalance in the pro- and anti-inflammatory cytokines may be responsible for periodontal breakdown through immune responses. This study aimed to determine the total amount, concentration and ratio of interleukin (IL)-11 and IL-17 in gingival crevicular fluid (GCF) of chronic periodontitis (CP) patients. MATERIALS AND METHODS: Forty CP patients and 20 healthy controls (C) were included. The CP group was divided into two subgroups in line with the probing depth (PD) in GCF-sampling sites (CPa: PD >or= 5 mm, CPb: PD

Fibrinolytic responses of human peritoneal fluid in laparoscopic cholecystectomy: a prospective clinical study.

BACKGROUND: The reduction in peritoneal fibrinolysis is believed to be the pathogenetic mechanism of adhesion formation. The general conclusion based on previous clinical and experimental studies is that laparoscopic procedures produce less adhesion formation. The association between this beneficial effect of laparoscopic cholecystectomy and peritoneal fibrinolytic changes is not clear. Therefore, the authors aimed to compare the effects of open and laparoscopic cholecystectomy on peritoneal fibrinolysis. For this purpose, fibrinolytic parameters in peritoneal fluid were investigated 24 h after laparoscopic and open cholecystectomies. METHODS: In a prospective clinical study, peritoneal fluid was sampled via a drain 24 h after laparoscopic (n = 10) and open (n = 9) cholecystectomies. Activities and concentrations of tissue plasminogen activator (tPA), plasminogen activator inhibitor type 1 (PAI-1), and tPA/PAI-1 complex were determined by enzyme-linked immunosorbent assay (ELISA) kits. RESULTS: In peritoneal fluids, tPA and tPA/PAI-1 complex concentrations were higher in the open cholecystectomy group (p = 0.009 and p < 0.001, respectively), but tPA activity and PAI-1 concentrations did not differ between the groups (p = 0.514 and p = 0.716, respectively). CONCLUSIONS: Fibrinolytic changes in peritoneal fluid have several similarities in open and laparoscopic cholecystectomies with regard to tPA activity and PAI-1 levels. However, higher tPA levels after the open procedure probably are secondary to more intense tissue handling leading to mesothelial release of tPA.

Sildenafil citrate as a phosphodiesterase inhibitor has an antioxidant effect in the blood of men.

BACKGROUND AND OBJECTIVE: Sildenafil citrate enhances the action of nitric oxide by preventing the hydrolysis of cGMP, and is widely used to treat erectile dysfunction. We investigated the effects of sildenafil citrate administration on lipid peroxidation and antioxidant redox enzymes in blood of healthy men. METHOD: Thirty healthy male subjects were divided equally into two groups. The first group was used as the control. A single dose of sildenafil citrate was administrated orally to subjects constituting the second group. Blood samples were obtained at 0, 2, 6 and 24 h after intake of the single dose of 100 mg sildenafil citrate or placebo. RESULTS AND DISCUSSION: The dose of sildenafil citrate resulted in significant increase in the erythrocyte superoxide dismutase and catalase activities at 6 and 24 h. Plasma lipid peroxidation levels decreased slightly. There was no statistical difference in erythrocyte glutathione peroxidase activity between the placebo and sildenafil citrate groups. CONCLUSION: Treatment of blood with 100 mg sildenafil citrate has protective effects on oxidative stress by inhibiting free radical formation and by supporting antioxidant redox systems.

Effects of intravenous N-acetylcysteine on periprocedural myocardial injury after on-pump coronary artery by-pass grafting.

AIM: Myocardial ischemia/reperfusion injury in patients undergoing coronary artery by-pass grafting (CABG) involves the reperfusion-induced conversion of reversible injured myocardial and endothelial cells. N-acetylcysteine (NAC) has a potential being the minimization of the impact of reperfusion injury. The aim of this study was to evaluate the effects of intravenous NAC on periprocedural myocardial injury after CABG. METHODS: The population of this prospective-randomized, double blind, placebo controlled study consisted of 40 patients undergoing on-pump CABG. All the patients were treated with standard medical therapy and eligible patients were randomized to NAC group (N.=19; intravenous infusion for 1 hour before the procedure at a dose of 50 mg/kg, followed by intravenous infusion for 48 hours after the operation at a dose of 50 mg/kg/day) and placebo (saline) group (N.=21). The study drug and placebo infusions were set to infuse at the same rate. RESULTS: Demographic and procedural variables were similar in the both groups (All P>0.05). Creatine kinase MB isoform (CK-MB) mass levels did not significantly differ between the groups at both preoperative and postoperative periods. Similarly, cTnT levels were similar in the groups at all periods. Eight patients in the NAC group and 7 in the placebo group had increased CK-MB >3 times normal value. However, only 3 patients in the NAC group experienced CK-MB>5 times normal value. CONCLUSION: Results of this study indicated that periprocedural use of NAC as intravenously did not attenuate myocardial damage after on-pump CABG surgery.

Gingival crevicular fluid leptin levels in periodontitis patients with long-term and heavy smoking.

BACKGROUND: The aim of the present study was to evaluate gingival crevicular fluid (GCF) leptin levels and the influence of long-term and heavy smoking on GCF leptin levels in patients with chronic periodontitis. METHODS: In this study, 143 individuals were divided into three groups: non-smokers (NS), smokers (S), and control (C). Three subgroups of NS and S were grouped as follows: a) probing depth (PD) 5 mm. For each patient, PD, gingival index (GI), plaque index (PI), gingival bleeding time index (GBTI), and clinical attachment level (CAL) values were recorded. The GCF leptin levels obtained from sampling sites were determined by using enzyme-linked immunosorbent assay kits. RESULTS: The GCF leptin levels were found significantly lower in the a and b subgroups in the S group than those in the NS group (P <0.05). The inflammatory markers GI and GBTI showed significant correlations with leptin in NS (P <0.05). CONCLUSIONS: Our results suggest that higher leptin GCF levels in healthy sites in periodontitis patients may play a protective role in periodontal disease. Further studies are needed to determine the cellular origin of the leptin in the gingiva and the effect of plasma leptin levels on GCF leptin concentrations.

The effects of organophosphate insecticide methidathion on lipid peroxidation and anti-oxidant enzymes in rat erythrocytes: role of vitamins E and C.

The effects of organophosphate insecticide methidathion (MD) on lipid peroxidation and anti-oxidant enzymes and the ameliorating effects of a combination of vitamins E and C against MD toxicity were evaluated in rat erythrocytes. Experimental groups were: control group, MD-treated group (MD), and MD + vitamin E + vitamin C-treated group (MD + Vit). MD and MD + Vit groups were treated orally with a single dose of 8 mg/kg MD body weight at 0 hour. Vitamins E and C were injected at doses of 150 mg/kg body weight, i.m. and 200 mg/kg body weight, i.p., respectively, 30 min after the treatment of MD in the MD + Vit group. Blood samples were taken 24 hours after the MD administration. The level of malondialdehyde (MDA), and the activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and catalase (CAT) were studied in the erythrocytes. MDA level increased significantly in the MD group compared to the control group (P < 0.05) and decreased significantly in the MD + Vit group compared to the MD group (P < 0.05). The activities of SOD, GSH-Px, and CAT decreased in the MD group compared to the control group (P < 0.05). Only GSH-Px activity increased in the MD + Vit group compared with the MD group. These results suggest that treating rats with MD increases LPO and decreases anti-oxidant enzyme activities in erythrocytes. Furthermore, single-dose treatment with a combination of vitamins E and C 30 min after the administration of MD can reduce LPO caused by MD.

The effect of lidocaine/prilocaine cream on an experimental wound healing model.

The effects of lidocaine/prilocaine cream on wound healing were evaluated in this study. An incisional wound model on abdominal wall was performed on mice. A full thickness skin incision 2 cm in length was performed then it was sutured primarily with 4/0 polypropylene. In group I (n = 10) only suturing was done (control group), in group II (n = 10) lidocaine cream was applied after suturing on wound site and it was repeated for 6 days (twice in a day), in group III (n = 10) lidocaine/prilocaine cream was applied topically after suturing and repeated 6 days (twice in a day). At day 7, incisions were excised for evaluating tensile strength and 5-hydroxyproline (5-HP) values. Tensile strength values were lowest in control group and highest in lidocaine/prilocaine treatment group. 5-HP values were also expressed the same results. Both tensile strength and 5-HP values increased significantly in treatment groups in regard to the control (p < 0.05). It was concluded that lidocaine/prilocaine cream as topical anaesthetic agent had no adverse effect in an incisional wound model, furthermore it may have some beneficial effects on wound healing which remains to be evaluated and it can be used safely in day-to-day emergency practices.

Lipid peroxidation and glutathione peroxidase activity in chronic obstructive pulmonary disease exacerbation: prognostic value of malondialdehyde.

Results of recent studies have indicated that during exacerbation of chronic obstructive pulmonary disease (COPD), antioxidant capacity is lower and the levels of lipid peroxidation products are higher than those in age-matched healthy subjects. The aim of this study was to assess the time course of changes in oxidant stress during the treatment of exacerbation of COPD. For this purpose, we measured erythrocyte glutathione peroxidase (GPx) activity and serum levels of the lipid peroxidation product malondialdehyde (MDA) in 18 male patients with acute exacerbation of COPD. Fifteen healthy non-smokers having no history of lung disease served as control subjects. Mean erythrocyte GPx values of patients were 45.54 +/- 9.04 u/gHb on admission and had increased to 72.77 +/- 9.68 by the tenth day of treatment, but still remained lower than those of healthy subjects (83.13 +/- 10.91) (p=0.007). Serum MDA values in patients were Vol. 12, No. 1, 2001 significantly higher (2.68 +/- 1.28 nmol/ml) than those in control subjects (1.04 +/- 0.36 nmol/ml) (p=0.000) and returned to normal values by the tenth day of treatment (1.08 +/- 0.36 nmol/ml) (p=0.766). Erythrocyte GPx values in patients who were current smokers (39.87 +/- 3.82 u/gHb) were lower than those in ex-smokers (49.15 +/- 9.67 u/gHb) (p=0.021). Moreover, serum MDA values in patients who were current smokers (3.32 +/- 1.18 nmol/ml) were higher than those in ex-smokers (1.66 +/- 0.60 nmol/ml) (p=0.007). The results show that oxidative stress in patients with acute exacerbation of COPD is related to higher MDA levels that return to normal conditions during the course of treatment. In conclusion, the results suggest that MDA levels can serve as a marker of prognosis and of the success of treatment of the exacerbation of COPD.

Polymorphic variants of MnSOD Val16Ala, CAT-262 C < T and GPx1 Pro198Leu genotypes and the risk of laryngeal cancer in a smoking population.

OBJECTIVE: To investigate the relationship between development of laryngeal cancer and the presence of polymorphisms of the MnSOD Val16Ala, CAT-262 C < T and GPx1 Pro198Leu genes in a smoking population. PATIENTS AND METHODS: Single nucleotide polymorphisms were determined in DNA from the peripheral blood erythrocytes of 48 heavy smokers (25 patients with laryngeal cancer and 23 cancer-free controls), using polymerase chain reaction. RESULTS: There were no significant differences in age, smoking duration or smoking intensity, comparing the two groups. The homozygous AA genotype of MnSOD Val16Ala was significantly more prevalent in the cancer group than the control group (92 vs 13 per cent, respectively), while the heterozygous AV genotype of MnSOD Val16Ala was more prevalent in the control group than the cancer group (87 vs 8 per cent, respectively) (p < 0.001). There were no significant differences between the cancer and control groups regarding GPx1 Pro198Leu or CAT-262 C < T polymorphisms. CONCLUSION: Polymorphism of the MnSOD Val16Ala gene may contribute to susceptibility to laryngeal cancer among smokers.

Methyl palmitate attenuates lipopolysaccharide-induced acute lung injury in mice.

AIM: The study is aimed to determine the beneficial effects of methyl palmitate (MP) which has antioxidant and anti-inflammatory effects demonstrated on murine model of acute lung injury induced by lipopolysaccharide (LPS). MATERIALS AND METHODS: Forty male BALB/C mice were randomly allocated into four groups (n=10, each): control group, methyl palmitate group (300 mg/kg), LPS group, and methyl palmitate -treated groups. Methyl palmitate or vehicle was given with an intraperitoneal administration 1 h before an intratracheal instillation of LPS (5 mg/kg). The severity of pulmonary injury was evaluated 6 h after LPS challenge. All experimental procedures complied with the requirements of the Animal Care and Ethics Committee of the Adnan Menderes University. RESULTS: Methyl palmitate pretreatment significantly attenuated LPS-induced pulmonary histopathologic changes, alveolar hemorrhage, and neutrophil infiltration. Methyl palmitate pretreatment also reduced the concentrations of malondialdehyde in lung tissues. CONCLUSIONS: This study indicates that methyl palmitate may have a protective effect against LPS-induced acute lung injury, and the potential mechanism of this action may involve the inhibition of NF-κB. activation.

Impairment of endothelium-dependent vasorelaxation in cadmium-hypertensive rats.

Abnormalities in the production and/or release of relaxing factors from the endothelium have been implicated in the development of hypertension in several animal models. Endothelium-dependent relaxation has been reported to be impaired in thoracic aorta in experimentally induced and genetically hypertensive rats. Present study has extented these observations to thoracic aorta of cadmium-hypertensive rats. The possible role of alterations in oxidant status was also studied. Hypertension was induced by the intraperitoneal administration of 1 mg/kg/day cadmium for 15 days. Mechanical responses produced by acetylcholine (ACh, 10(-9)-10(-4) M) and sodium nitroprusside (SNP, 10(-10)-10(-5) M) were studied on phenylephrine-precontracted thoracic aorta rings from control and cadmium-hypertensive rats. Serum nitric oxide (NO) and aortic malondialdehyde (MDA) levels were measured. ACh-induced relaxation was attenuated in aorta from cadmium-hypertensive rats, whereas relaxation responses to SNP did not differ significantly between the groups. Exposure of aortic rings to N(G)-nitro-L-arginine methyl ester (L-NAME, 10(-4) M) resulted in a significantly greater inhibition of relaxation response to ACh in aortic rings of cadmium-hypertensive rats as compared with control rats. Incubation with L-arginine (L-Arg, 10(-3) M) caused a similar reversal of the inhibition of ACh-induced relaxation by L-NAME in both groups. Serum NO levels were decreased and aortic MDA levels were increased in cadmium-treated rats as compared with control rats. However, the differences between the groups did not reach a statistical significance. These findings suggested that the reduction in endothelium-dependent relaxation may play a role in cadmium-induced hypertension as it was in many other hypertension models.

The effects of diazinon on lipid peroxidation and antioxidant enzymes in rat heart and ameliorating role of vitamin E and vitamin C.

Diazinon is one of the most widely used organophosphate insecticides (OPIs) in agriculture and public health programs. Reactive oxygen species (ROS) caused by OPIs may be involved in the toxicity of various pesticides. The aim of this study was to investigate how diazinon affects lipid peroxidation (LPO) and the antioxidant defense system in vivo and the possible ameliorating role of vitamins E and C. For this purpose, experiments were done to study the effects of DI on LPO and the activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and catalase (CAT) in adult rat heart. Experimental groups were: (1) control group, (2) diazinon treated (DI) group, (3) DI+vitamins E and C-treated (DI+Vit) group. The levels of malondialdehyde (MDA) and the activities of SOD and CAT increased significantly in the DI group compared with the control group. The activity of SOD and the levels of MDA decreased significantly in the DI+Vit group compared with the DI group. The differences between the DI+Vit and control groups according to the MDA levels and the activities of both SOD and CAT were statistically significant. These results suggest that treating rats with a single dose of diazinon increases LPO and some antioxidant enzyme activities in the rat myocardium and, in addition, that single-dose treatment with a combination of vitamins E and C after the administration of diazinon can reduce LPO caused by diazinon, though this treatment was not sufficiently effective to reduce the values to those in control group.

The effects of subchronic methidathion toxicity on rat liver: role of antioxidant vitamins C and E.

Methidathion (MD) phosphorodithioic acid S-[(5-methoxy-2-oxo-1,3,4-thiadiazol-3(2H)-yl)methyl] O,O-dimethyl ester is the organophosphate insecticide (OPI) most commonly used worldwide in the pest control of crops. Subchronic MD exposure was evaluated for its effects on lipid peroxidation, the serum activities of cholinesterase (ChE), and enzymes concerning liver damage, and the protective effects of combination of vitamins E and C in albino rats. Additionally, the histopathological changes in liver tissue were examined. Experimental groups were as follows: control group; a group treated with 5 mg/kg body weight MD (MD group); and a group treated with 5 mg/kg body wight MD plus vitamin E plus vitamin C (MD+AO group). The MD and MD+AO groups were treated orally with MD on five days a week for 4 weeks. The serum activities of cholinesterase (ChE), alanine transferase (ALT), aspartate amiotransferase (AST), lactate dehydrogenase (LDH), gamma-glutamyltransferase (GGT), alkaline phosphatase (ALP), and the concentration of malondialdehyde (MDA) and liver histopathology were studied. In serum samples, MD significantly increased MDA concentration and ALP, AST, GGT, LDH activities but decreased the ALT and ChE activities. In the MD+AO group, MDA level and ALP, AST, LDH activities were significantly decreased and ChE activity was increased compared to the MD group. Histopathological changes found in liver tissue of rats treated with MD included were infiltration with mononuclear cells in all portal areas, sinusoidal dilatation, and focal microvesicular steatosis and hydropic degenerations in parenchymal tissue. The severity of these lesions was reduced by administration of vitamins. From these results, it can be concluded that subchronic MD causes liver damage, and lipid peroxidation may be a molecular mechanism involved in MD-induced toxicity. Furthermore, the combination of vitamins E and C can reduce the toxic effects of MD on liver tissue of rats.