PurposeNon-steroidal anti-inflammatory drugs (NSAID) are frequently used in oral surgical procedures in dentistry. The evaluation of the frequency of sister chromatid exchange (SCE) is accepted as a reliable cytogenetic method to assess the genotoxic effects of environmental factors.Materials and MethodsIn this study, the genotoxic effects of various NSAIDs were assessed in 30 patients to who they were administered following encluosed third molar surgery using SCE analysis before and after the operation. The frequency of SCE was evaluated before the operation and after 3 days of etodolac, nimesulid and naproxen use.ResultsThere was no statistically significant difference in the frequency of SCE between the preoperative and postoperative states in patients given etodolac, nimesulid or naproxen sodium.ConclusionShort term use of selective and non-selective NSAIDs was not associated with a significant genotoxic effect that could be detected using the SCE method in peripheric lymphocytes.
Obesity is a major risk factor for insulin resistance and type 2 diabetes mellitus (T2DM). Resistin, an adipocyte-secreted hormone, is thought to take a part in the development of insulin resistance and T2DM. The aim of this study was to characterise the changes in circulating levels of resistin and proinflammatory cytokines tumour necrosis factor-alpha (TNF-alpha) and interleukin (IL)-6 in diabetic and prediabetic obese patients and to explore their relationship to insulin resistance. Attempts were also made to see whether resistin levels are related to the degree of oxidative stress, as determined by the measurement of advanced oxidation protein products (AOPPs). The study groups consisted of obese diabetic (BMI: 30-42 kg/m(2), n=28) and prediabetic (BMI: 29-41 kg/m(2), n=23) women. Fourteen healthy women, with BMI in the range 21.5-25.5 kg/m(2), were taken as controls. Serum levels of TNF-a, IL-6, resistin, glucose, insulin and AOPPs were measured. Insulin resistance was calculated by the homeostasis model assessment (HOMA-IR). Diabetic and prediabetic obese patients had increases in serum resistin and TNF-alpha levels (P<0.01 and P<0.001, respectively). IL-6 levels in diabetic patients were significantly higher than in prediabetics (P<0.05). AOPP levels were also significantly higher in diabetics than prediabetics and controls (P<0.05 and P<0.001, respectively); and positively correlated with blood glucose. Insulin was significantly associated with circulating resistin and TNF-alpha. The development of insulin resistance may contribute to the elevation of circulating resistin or vice versa. Determination of AOPPs may be helpful for monitoring the impaired glucose metabolism in obesity.
Estrogen deficiency alone may not cause an increase in ADMA levels unless the women are prone to disturbances in energy homeostasis. In spite of the high ADMA levels, the unaltered NO levels in plasma may be owing to ongoing inflammatory conditions.
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