Airway inflammatory markers in chronic obstructive pulmonary disease patients and healthy smokers.

BACKGROUND: Cigarette smoke with its toxic ingredients leads to chronic inflammations in the airways. OBJECTIVES: In this study, the effect of cigarette smoke on the levels of inflammatory markers, interleukin-6 (IL-6), interleukin-8 (IL-8), and tumor necrosis factor-alpha (TNF-α) in induced sputum was investigated. MATERIALS AND METHODS: Twenty patients with chronic obstructive pulmonary disease (COPD) (group I), 20 healthy smokers (group II), and 20 healthy nonsmokers (group III) were included in the study. The levels of IL-6, IL-8, and TNF-α in induced sputum were measured in these groups, and comparison analysis between the groups and correlation analysis for smoking load (pack-years) and spirometric parameters were performed. RESULTS: Mean age of the patients in groups I, II, and III were 61.2 ± 1.7, 58.2 ± 1.6, and 59.1 ± 5.4 years, respectively (P > 0.05). Smoking loads of group I and group II were 38.6 ± 2.1 and 29.5 ± 2.3 pack-years, respectively (P < 0.05). All cytokine levels were significantly higher in group I than groups II and III (P < 0.05). In addition to this, mean cytokines levels were significantly higher in group II than group III (P < 0.05). Smoking load of group II subjects was positively correlated with IL-6, IL-8, and TNF-α in induced sputum (P < 0.05). CONCLUSIONS: We found that inflammatory marker levels in induced sputum were significantly higher in COPD patients and smokers than nonsmokers. Moreover, there was a moderate positive correlation between IL-6, IL-8, and TNF-α levels and smoking load in the healthy smokers. We think that further studies are needed to determine whether higher levels of cytokine levels in sputum might be helpful in predicting the healthy smokers who will develop COPD in future.

The effects of Gingko biloba, vitamin E and melatonin on bacterial translocation in thioacetamide-induced fulminant hepatic failure in rats.

BACKGROUND AND STUDY AIMS: Bacterial translocation (BT) has been implicated in the development of infectious complications in many serious clinical conditions such as fulminant hepatic failure (FHF). We aimed to investigate the effects of Gingko biloba (GB), vitamin E (Vit E) and melatonin on intestinal oxidative damage and BT in thioacetamide (TAA)-induced FHF in rats. MATERIALS AND METHODS: A total of 42 rats were divided into five groups. Group 1 (n = 8) was the control group. Group 2 (n = 10) was the TAA group, in which rats received 350 mg/kg TAA daily by the intraperitoneal (ip) route for 3 days. Oral 100 mg/kg GB per day was administered to group 3 (n = 8), oral 200 mg/kg Vit E per day to group 4 (n = 8) and ip 3 mg/kg melatonin per day to group 5 (n = 8) 48 h prior to the first TAA injection and was continued for 5 consecutive days. RESULTS: When compared with the control group, serious hepatic and intestinal oxidative damage, increased Escherichia coli counts in ileal aspirates and high BT frequencies were observed in the TAA group (all p < 0.0001). Only GB treatment attenuated hepatic oxidative damage (p < 0.0001). There was no difference in intestinal oxidative damage, E. coli counts in ileal aspirates and BT frequency between TAA and the other antioxidant treatment groups (p > 0.05). CONCLUSION: Our results suggest that intestinal oxidative damage plays a major role in the development of BT by disrupting the barrier function of intestinal mucosa.

Protective effects of Gingko biloba on thioacetamide-induced fulminant hepatic failure in rats.

Gingko biloba (GB) has antioxidant and platelet-activating factor (PAF) antagonistic effects. We investigated the protective effects of GB on thioacetamide (TAA)-induced fulminant hepatic failure in rats. Fulminant hepatic failure was induced in treatment groups by three intraperitoneal (ip) injections of TAA (350 mg/kg) at 24-hour intervals. Treatments with GB (100 mg/kg per day, orally) and N-acetylcysteine (20 mg/kg twice daily, sc) were initiated 48 hours prior to TAA administration. The liver was removed for histopathological examinations. Serum and liver thiobarbituric acid-reactive substance (TBARS) levels were measured for assessment of oxidative stress. Liver necrosis and inflammation scores and serum and liver TBARS levels were significantly higher in the TAA group compared to the control group (P < 0.001, < 0.001, 0.001, < 0.001, respectively). Liver necrosis and inflammation scores and liver TBARS levels were significantly lower in the GB group compared to the TAA group (P < 0.001, < 0.001 and 0.01, respectively). GB ameliorated hepatic damage in TAA-induced fulminant hepatic failure. This may be due to the free radical-scavenging effects of GB.

Serum nitrate and nitrite levels in patients with rheumatoid arthritis, ankylosing spondylitis, and osteoarthritis.

OBJECTIVE: To assess and compare serum nitrate and nitrite levels in patients with ankylosing spondylitis (AS), rheumatoid arthritis (RA), and osteoarthritis (OA). METHODS: Thirty five patients with RA, 32 patients with AS, and 36 patients with OA were entered into this study. In addition, 30 healthy volunteers acted as a control group. Concentrations of nitrate and nitrite in serum were determined by direct and indirect Griess reactions. C reactive protein and erythrocyte sedimentation rate levels were determined as markers of systemic activity of disease (SAD) in RA and AS groups. RESULTS: Serum nitrate and nitrite levels were found to be higher in patients with AS and RA than in the OA group (p<0.01). In addition, serum nitrate and nitrite levels were higher in all three groups than in the control group (p<0.01). Moreover, serum nitrate and nitrite levels were higher in patients who had SAD than in those who had not in the RA and AS groups (p<0.01 and p<0.05, respectively), and there was a correlation between serum nitrate and nitrite concentrations and SAD variables in patients with RA (Spearman's r(s)=0.414, p<0.05 and r(s)=0.408, p<0.05, respectively) and AS (r(s)=0.421, p<0.05 and r(s)=0.412, p<0.05, respectively). CONCLUSION: The findings suggest that nitrate and nitrite production is enhanced in patients with inflammatory arthritis compared with OA. In addition, serum nitrate and nitrite levels are enhanced in patients with RA, AS, and OA compared with healthy subjects. Furthermore, there is a correlation between the SAD variables and serum nitrate and nitrite levels in patients with RA and AS.

Investigation of serum minimal inhibitory concentrations of some benzimidazole, imidazole and benzothiazole derivatives and their effects on liver and renal functions.

In previous studies many benzimidazole, imidazole and benzothiazole derivatives had been synthesized and their antimicrobial activities were tested in vitro conditions. Four of these compounds showed minimal inhibitory concentrations (MIC) of 5-25 micrograms/ml against standard strains and clinical isolates. In order to determine whether these four compounds can be used for therapeutic purpose, their serum MIC values and side effects on hepatic and renal functions were determined. Different concentrations of the compounds were tested on Wistar rats. Compound 1 was administered orally, intramuscularly and intravenously; compounds 2, 3 and 4 were given orally and intramuscularly. Blood samples were taken 4 and 24 h after administration of the compounds. Serum MIC values were investigated by bioassay and serum levels of biochemical parameters by autoanalyzer. None of the tested compounds showed antimicrobial activity at their serum concentrations. Although creatinine activity was found at normal levels in all experiments, compounds 1 and 2 caused a significant increase in blood urea nitrogen (BUN) level. The values of aspartate aminotransferase and/or alanine aminotransferase and/or alkaline phosphatase which are characteristic for liver function were generally found at high levels. According to these results, it can be concluded that the tested compounds caused damage in liver and biliary tracts without antimicrobial activity by their serum concentrations.