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There is growing evidence that oxidative stress contributes to the pathogenesis of anxiety disorders. Our aim was to measure oxidative stress in anxiety disorders subjects, and assesses the potential confounding influences of anti anxiety therapy. Serum malondialdehyde and antioxidant levels were estimated in patients at the time of presentation and also after anti- anxiety therapy for 3 months. During the period of study no antioxidant/s was given to the patients and control subjects. Serum malondialdehyde levels were significantly higher in the anxiety disorders patients in comparison to control cases. Also, the antioxidant activity of enzymes super oxide dismutase, glutathione and non enzymatic antioxidant levels of vitamins E and C were significantly lower in patients compared to controls at the initial presentation. After 3 months of anti anxiety treatment all the above parameters showed reversal in the respective levels of serum malondialdehyde and antioxidant activity. Anti anxiety medications results in reduced oxidative stress which indicates that oxidative stress is not the cause, but rather a consequence, of anxiety disorders.

Kinetics of Pd(II) catalyzed oxidation of valine has been studied by N-bromophthalimide (NBP) in acidic me- dium at 303 K. The reaction follows first order kinetics with respect to (Pd(II)) while negative effect was observed for the variation of (H + ) on the rate of reaction. The reaction exhibits first order kinetics with respect to (NBP) at its lower con- centrations and tends towards zero order at its higher concentrations. Rate of reaction exhibits zero order and fractional order kinetics with respect to (valine) and (Cl - ) respectively. (Hg(OAc)2), (phthalimide), ionic strength (I) and dielectric constant of the medium did not bring about any significant change on the rate of reaction. The rate constants observed at five different temperatures (298 K-318 K) were utilized to calculate the activation parameters. A plausible mechanism has been proposed from the results of kinetic studies, reaction stoichiometry and product analysis.

Objective: To access the oxidative stress status by quantification of byproducts generated during lipid peroxidation and DNA breakdown products generated during DNA damage in the blood serum of multiple myeloma and lymphoma patients. Material & Methods: Case control study comprised of 40 patients of multiple myeloma and 20 patients of lymphoma along with 20 age and sex-matched healthy subjects as controls. Levels of Malondialdehyde and 8-hydroxy-2-deoxy-Guanosine were measured to study the oxidative stress status in the study subjects. Results: The level of markers of DNA damage and lipid peroxidation were found to be raised significantly in the study subjects in comparison to healthy controls. The results indicate oxidative stress and DNA damage activity increase progressively with the progression of disease. Conclusion: Oxidative stress causes DNA damage and Lipid peroxidation which results in the formation of DNA adducts leading to mutations thereby indicate the role of oxidative stress in the pathogenesis of multiple myeloma and lymphoma.