Meral Yuksel

Obstructive sleep apnea syndrome is characterized by repetitive obstruction of the upper airways, and it is a risk factor for cardiovascular diseases. There have been several studies demonstrating low levels of nitric oxide in patients with obstructive sleep apnea syndrome compared with healthy controls. In this study, we hypothesized that reduced nitric oxide levels would result in high arginase activity. Arginase reacts with L-arginine and produces urea and L-ornithine, whereas L-arginine is a substrate for nitric oxide synthase, which produces nitric oxide. The study group consisted of 51 obstructive sleep apnea syndrome patients (M/F: 43/8; mean age 49±10 years of age) and 15 healthy control subjects (M/F: 13/3; mean age 46±14 years of age). Obstructive sleep apnea syndrome patients were divided into two subgroups based on the presence or absence of cardiovascular disease. Nitric oxide levels and arginase activity were measured via an enzyme-linked immunosorbent assay of serum samples. Serum nitric oxide levels in the control subjects were higher than in the obstructive sleep apnea patients with and without cardiovascular diseases (p<0.05). Arginase activity was significantly higher (p<0.01) in obstructive sleep apnea syndrome patients without cardiovascular diseases compared with the control group. Obstructive sleep apnea syndrome patients with cardiovascular diseases had higher arginase activity than the controls (p<0.001) and the obstructive sleep apnea syndrome patients without cardiovascular diseases (p<0.05). Low nitric oxide levels are associated with high arginase activity. The mechanism of nitric oxide depletion in sleep apnea patients suggests that increased arginase activity might reduce the substrate availability of nitric oxide synthase and thus could reduce nitric oxide levels.

Obstructive sleep apnea syndrome (OSAS) is associated with increased cardiovascular morbidity and mortality. We aimed to investigate the matrix metalloproteinase-9 (MMP-9) level and MMP-9 gene polymorphism in sleep apnea patients with or without cardiovascular disease. Case-control study. Two hundred nine patients [Mean age (±SD), 47 (±12) yrs; M/F, 170/39] diagnosed with sleep-disordered breathing were included in the study. Serum MMP-9 level was performed using enzyme-linked immunosorbant assay (ELISA) and MMP-9 gene polymorphism with polymerase chain reaction-restriction fragment length polymorphism. We divided the patient group into two subgroups: (1) patients with confirmed cardiovascular disease, i.e. CV-P Group and (2) patients without cardiovascular disease, CV-N Group. We compared all parameters between the two groups. There were 56 OSAS patients with cardiovascular disorder (CV-positive group) and 153 OSAS patients without cardiovascular disorder (CV-negative group). CC, CT and TT genotype distributions between groups were similar [31 (55%), 25 (45%), 0 (0%) vs 88 (57%), 61 (40%), 4 (3%); respectively, p>0.05]. MMP-9 level was significantly higher in CV-P patients (442.7±139.3 pg/mL) than in CV-N patients (364.4±165.0 pg/mL; p=0.0018). Our results showed that the presence of MMP-9 polymorphism was not associated with cardiovascular disease. MMP-9 level was higher in OSAS patients with cardiovascular disorders than without cardiovascular disorders. Finally, MMP-9 genotype was not associated with serum MMP-9 levels.

Different types of reactive oxygen metabolites (ROMs) are known to be involved in carcinogenesis. Several studies have emphasized the formation of ROMs in ischemic tissues and in cases of inflammation. The increased amounts of ROMs in tumor tissues can either be because of their causative effects or because they are produced by the tumor itself. Our study aimed to investigate and compare the levels of ROMs in tumor tissue and adjacent lung parenchyma obtained from patients with lung cancer.

Acrylamide (ACR) is a vinyl monomer with a significantly high chemical reactivity. It is easily absorbed by all routes of administration and peripheral nervous system is a selective target for its toxicity. The early clinical symptoms to ACR results in degeneration of nerves causing distal axonopathy. ACR has been reported to cause disturbances in oxidative stress. The aim of this study is to determine the effects of alpha lipoic-acid (LA) and n-acetyl cysteine (NAC) against acrylamide-induced peripheric neuropathy in rats. Male Sprague-Dawley rats were included in the study. ACR was given i.p. at a dose of 45mg/kg/day. LA group received additionally 35mg/kg/day LA, and NAC group received 150mg/kg/day NAC for 10 days. Controls were injected saline at the same dose. After the time rats were sacrified and sciatic nerves were removed. For free radical determination luminol (selective for hydroxyl radical, hydrogen peroxide and hypochlorous acid) and lucigenin (selective for superoxide radical) enhanced chemiluminescence (CL) method was used. Additionally histopathological examination was also made. Our luminol enhanced CL results was in ACR group higher than control group (21,6±7,1rlu/mg tissue vs. 11,2±1,9rlu/mg tissue;p<0,001). LA and NAC reduces luminol enhanced CL (8,6±1,7rlu/mg tissue vs. 9,5±2,2rlu/mg tissue) measurements significantly (p0.05). LA has a low reducing effect but was also not significantly. Histopathological examination has shown normal myelination in peripheric neurons. In ACR group myelin organization was damaged and the count of disturbed myelinated nerve fibers was increased with respect to the control group. NAC and LA groups has shown a moderate reducing effect against myelin damage. ACR toxicity increased oxidative stress in peripheric neurons, which results with myelin damage. NAC and LA can reduce this damage. In conclusion, LA and NAC has protective effects against ACR induced peripheric neuropathy.