ABSTRACT
The aim of the study is to levels of nicotine and cotinine were elevated the oxidative stress malondialdehyde (MDA) and inflammation as nitric oxide (NO2 and NO3) may possibly be associated with decreased antioxidant enzyme activities and can sensitively indicate the production of reactive oxygen species (ROS). To evaluate the quantitative analysis of nicotine and cotinine levels and the alterations in the selected parameters of antioxidant metabolisms during nitroxidative stress in the saliva of smokeless tobacco consumers. Saliva nicotine and cotinine was measured by HPLC method and nitric oxide, lipid peroxidation and activities of antioxidant enzymes were estimated by spectrophotometric methods. Significant increase in concentrations of nicotine and cotinine levels of saliva in smokeless tobacco users in comparison to controls. Saliva lipid peroxidation was increased in experimental subjects (gutkha group 39.28% and khaini group 25.00%) as compared to controls and nitric oxide in the form of nitrites and nitrates was significantly increased in the saliva of smokeless tobacco users compared to controls. The activity levels of antioxidant enzymes were decreased in the saliva of the smokeless tobacco users in comparison with normal controls. A strong positive correlation of nicotine and cotinine with nitroxidative stress markers in gutkha and khaini users. Increased expression of inducible nitric oxide synthase (iNOS) enzyme leads to intoxication in saliva and indirectly induces inflammation process. Increased production of reactive oxygen species (ROS) and decrease in the activity levels of antioxidant enzymes in the saliva of smokeless tobacco users indicate conspicuous cell and tissue damage.
ABSTRACT
Oxidative stress is a common mediator in pathogenicity of established cardiovascular risk factors. Furthermore, it likely mediates effects of emerging, less well-defined variables that contribute to residual risk not explained by traditional factors. Functional oxidative modifications of cellular proteins, both reversible and irreversible, are a causal step in cellular dysfunction. Identifying markers of oxidative stress has been the focus of many researchers as they have the potential to act as an "integrator" of a multitude of processes that drive cardiovascular pathobiology. One of the major challenges is the accurate quantification of reactive oxygen species with very short half-life. Redox-sensitive proteins with important cellular functions are confined to signalling microdomains in cardiovascular cells and are not readily available for quantification. A popular approach is the measurement of stable by-products modified under conditions of oxidative stress that have entered the circulation. However, these may not accurately reflect redox stress at the cell/tissue level. Many of these modifications are "functionally silent". Functional significance of the oxidative modifications enhances their validity as a proposed biological marker of cardiovascular disease, and is the strength of the redox cysteine modifications such as glutathionylation. We review selected biomarkers of oxidative stress that show promise in cardiovascular medicine, as well as new methodologies for high-throughput measurement in research and clinical settings. Although associated with disease severity, further studies are required to examine the utility of the most promising oxidative biomarkers to predict prognosis or response to treatment.