Markers of Oxidative Stress in Generalized Anxiety Psychiatric Disorder: Therapeutic Implications

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

Lipid Peroxidation and Thymidine Phosphorylase expression in Prostate Carcinoma

Aim: To understand the association between markers of oxidative stress and angiogenesis in relation to disease progression, clinical stage and cytological grade in patho-physiology of prostate carcinoma.Patients and Methods: Case control study comprised of 50 prostate carcinoma patients along with 20 age and sex-matched healthy subjects as controls. Levels of malondialdehyde were measured to study the oxidative stress status in the study subjects. Angiogenesis was evaluated by studying the activity of Thymidine Phosphorylase/Platelet derived endothelial cell growth factor.Results: The levels of markers of oxidative stress along with the activity of thymidine phosphorylase were found to be significantly higher in the study subjects in comparison to healthy controls. The results indicate oxidative stress and angiogenesis activity increase progressively with the increase in staging and progression of disease.Conclusion: Oxidative stress and expression of angiogenesis activity points clearly that with the progression of oxidative stress there is a simultaneous progression of angiogenesis in relation to disease progression, clinical stage and cytological grade in the pathophysiology of prostate carcinoma

Oxidative Stress Induced Lipid Peroxidation And DNA Adduct Formation In The Pathogenesis Of Multiple Myeloma And Lymphoma

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

Protein Damage and Antioxidant Status Alterations Caused by Oxidative Injury in Chronic Myeloid Leukemia

Objective: To evaluate the oxidative stress and antioxidant defense in patients with chronic myeloid leukemia.Background: Chronic myeloid leukemia is a myeloproliferative disorder associated with a characteristic chromosomal translocation called the Philadelphia chromosome. Reactive oxygen species and other free radicals mediate phenotypic and genotypic changes leading from mutation to neoplasia in all cancers, including chronic myeloid leukemia. We evaluated patients with chronic myeloid leukemia by observing their oxidative status and antioxidant defense.Methods: Using serum from 40 clinically diagnosed cases of chronic myeloid leukemia as well as 40 healthy controls, we measured the concentration of thiobarbituric acid, levels of protein carbonylation, total antioxidant status, catalase, superoxide dismutase, glutathione peroxidase, vitamins A and E, and the trace elements zinc, magnesium, and selenium. Results: We found significantly increased levels of serum malonyldialdehyde and protein carbonyl in patients with chronic myeloid leukemia in comparison to healthy individuals, and significantly decreased levels of the antioxidants and micronutrients thiobarbituric acid, catalase, superoxide dismutase, glutathione peroxidase, vitamins A and E, zinc, magnesium, and selenium. These data suggest cellular damage occurring at the level of lipids and proteins.Conclusion: These findings indicate a link between low levels of antioxidants and cellular damage in patients with chronic myeloid leukemia, supporting the idea that oxidative stress may play a role in the pathogenesis of chronic myeloid leukemia

Vascular Endothelial Growth Factor Levels in Relation to Oxidative Damage and Antioxidant Status in Patients with Breast Cancer

Purpose: Oxidative stress and angiogenesis are important elements in the pathogenesis of inflammatory diseases and cancer. Vascular endothelial growth factor (VEGF) is one of the most potent angiogenic cytokines and is up-regulated by conditions associated with the generation of free radicals and reactive oxygen intermediates. In this study, we investigated the association between oxidative stress and serum VEGF status in patients with breast cancer. Methods: Forty patients with breast carcinoma, of which 21 were stage II and 19 were stage III, along with 40 ageand gender-matched healthy controls were enrolled. Oxidative stress, total antioxidant status, and VEGF levels in serum were evaluated by spectrophotometric procedures. Malondialdehyde (MDA) levels were measured and antioxidant status was assessed by measuring total antioxidant status (TAS) to assess oxidative damage. Results: VEGF and MDA levels were significantly higher i

Idiopathic localized involutional lipoatrophy: A retrospective study of 12 cases

Background: Idiopathic localized involutional lipoatrophy (ILIL) is focal loss of subcutaneous tissue without any clinical or histopathological inflammation with spontaneous regression. Objective: To retrospectively study clinical features and evolution of lesions in patients diagnosed with idiopathic localized lipoatrophy presenting to the department of dermatology of two district hospitals of Himachal Pradesh. Materials and Methods: A retrospective study of clinical patterns and evolution of ILIL was done in patients presenting with this condition in two district hospitals in the past 4 years (October 2013–September 2017). All clinically suspected and histopathologically confirmed cases of idiopathic localized lipoatrophy were included in the study. All cases with history of antecedent injections, vaccination, or medications before the development of lesion and inflammatory lipoatrophy on histopathology were excluded. Results: We found a total of 12 patients with ILIL. About 66% were children (8/12), 3 (25%) young females, and 1 (8%) young adult male. The most common site involved was buttock in 9 (75%) cases followed by a single case each (8%) with lesion on arm, face, and lower back. Two children and one adult were having bilateral involvement (25%), whereas the remaining had unilateral lesions. Lipoatrophy in 8 (66%) patients decreased spontaneously (with placebo) within 4–12 weeks duration whereas 4 required treatment. None required surgical or cosmetic interventions. Limitations: Small sample size and nonavailability of immunohistochemistry reports in all patients. Conclusion: ILIL is a rare form of lipoatrophy with specific loss of adipose tissue without any inflammatory changes. We concluded that ILIL is an underreported entity, probably due to its spontaneous resolution

The protein tyrosine phosphatase, nonreceptor type 22-1858C->T (rs2476601) polymorphism is not a genetic risk factor for systemic lupus erythematosus in Indian Tamils

Background: Systemic lupus erythematosus (SLE), a systemic autoimmune disease, occurs due to disruption of immune homeostasis against self-antigens. The etiology of SLE is complex and multiple genetic factors contribute to disease susceptibility and clinical phenotypes. Protein tyrosine phosphatase, nonreceptor type 22 (PTPN22) is a lymphoid-specific phosphatase that negatively regulates T-cell receptor signaling and is responsible for the maintenance of T-cell homeostasis. Genetic aberrations affecting the function of PTPN22 result in the proliferation of autoreactive T-cells and development of autoimmune diseases. Methods: We carried out a case–control genetic study to analyze the association of PTPN22 R620W polymorphism (rs2476601) with disease susceptibility and clinical and autoantibody profile in Indian Tamils with SLE. Three hundred SLE patients satisfying the 1997 revised American College of Rheumatology classification criteria for SLE were enrolled in the study. Disease activity was measured using the SLE Disease Activity Index. We recruited 460 age-, sex-, and ethnicity-matched individuals without a family history of autoimmune diseases as control population. Genomic DNA was extracted from the blood sample by salting-out method. The PTPN22-1858C->T (rs2476601) polymorphism was screened by polymerase chain reaction-restriction fragment length polymorphism. Results: The frequency of the ancestral allele “C” was similar in both cases and controls (99.3% and 99.8%, respectively) and the mutant allele “T” was less frequent in South Indian Tamil population; it did not influence clinical or serological phenotypes. Conclusion: Our findings suggest that the PTPN22 (rs2476601) polymorphism is less frequent and did not confer a risk for lupus or its associated clinical or serological phenotypes in South Indian Tamils

A novel approach to study oxidative stress in neonatal respiratory distress syndrome

Background: Respiratory distress syndrome of the neonate (neonatal RDS) is still an important problem in treatment of preterm infants. It is accompanied by inflammatory processes with free radical generation and oxidative stress. The aim of study was to determine the role of oxidative stress in the development of neonatal RDS. Methods: Markers of oxidative stress and antioxidant activity in umbilical cord blood were studied in infants with neonatal respiratory distress syndrome with reference to healthy newborns. Results: Status of markers of oxidative stress (malondialdehyde, protein carbonyl and 8-hydroxy-2-deoxy guanosine) showed a significant increase with depleted levels of total antioxidant capacity in neonatal RDS when compared to healthy newborns. Conclusion: The study provides convincing evidence of oxidative damage and diminished antioxidant defenses in newborns with RDS. Neonatal RDS is characterized by damage of lipid, protein and DNA, which indicates the augmentation of oxidative stress. General significance: The identification of the potential biomarker of oxidative stress consists of a promising strategy to study the pathophysiology of neonatal RDS

Sodium Dodecyl Sulphate-Supported Nanocomposite as Drug Carrier System for Controlled Delivery of Ondansetron

Sodium dodecyl sulphate-supported iron silicophosphate (SDS/FeSP) nanocomposite was successfully fabricated by the co-precipitation method. The SDS/FeSP nanocomposite was investigated as a drug carrier for ondansetron. The cumulative drug release of ondansetron was observed at various pH values for different time intervals, i.e., from 20 min to 48 h. A ranking of the drug release was observed at different pHs; pH 2.2 > saline (pH 5.5) > pH 7.4 > pH 9.4 > distilled water. Maximum release of encapsulated drug was found to be about 45.38% at pH 2.2. The cell viability tests of SDS/FeSP nanocomposite concluded that SDS/FeSP nanocomposite was non-cytotoxic in nature