Assessment of Role and Efficacy of Curcumin and Quercetin in Preventing Lead-Induced Oxidative Stress in Rats.

Lead (Pb) is found in almost all phases in environment and biological systems. Pb stimulated oxidative stress is a state that involves the generation of free radicals beyond the permissible limits, which can deplete the antioxidant reserves and can result in oxidative stress, thus hampering the ability of the biological system to reverse the result. Exposure of rats to Pb (25 mg/kg body weight) for 8 weeks caused an increase in Pb levels in blood and brain. Activity of delta-aminolevulinic acid dehydratase (δ-ALAD) and antioxidant enzymes such as Superoxide dismutase (SOD) and Catalase (CAT) decreased in the blood of Pb-treated group with a concomitant increase in the level of lipid peroxidation (LPO) and no significant change in the level of reduced glutathione (GSH) level was found. Interestingly, co-treatment of Pb-treated rats with curcumin (30 mg/kg body weight) and quercetin (30 mg/kg body weight) for 8 weeks caused a significant decrease in Pb levels of blood and all brain regions versus those treated with Pb alone. A significant improvement in levels of MDA, δ-ALAD, SOD and CAT activities was observed in rats simultaneously treated with curcumin or Quercetin or both with lead. Therefore, the ameliorative impact of curcumin and Quercetin might be due to their antioxidant property hence were able to counter the oxidative stress generated by Pb. These results suggest that combination of curcumin and Quercetin could be utilized as a possible supplement with the relevant therapeutics in the suitable management of Pb toxicity.

Genetic polymorphism of tumor necrosis factor alpha (TNF-α) and tumor necrosis factor beta (TNF-ß) genes and risk of oral pre-cancer and cancer in North Indian population.

OBJECTIVE: There are inconclusive data connecting single-nucleotide polymorphisms (SNPs) of TNF-α (rs361525) and TNF-ß (rs909253) to potential malignant oral disorder (PMOD) such as lichen planus and oral fibrosis. Here, we have investigated the risk of oral squamous cell carcinoma as well as oral pre-cancerous lesions in North Indian population with the polymorphism of the TNFα/ ß genes. MATERIAL AND METHODS: A total 500 patients with oral pre-cancer and OSCC and 500 healthy volunteers were genotypes for the TNF-α (-238) G/A (rs361525) and TNF-ß (252) A/G (rs909253) gene polymorphism. Genotypes were identified by polymerase chain reaction (PCR) restriction fragment length polymorphism (RFLP). Genotype frequencies were evaluated by Chi-square test. RESULTS: Compared to the GG genotype, the GA genotype of TNF-α (G238A) polymorphism (rs361525) has been found to significantly increase the risk of oral disease (OR = 1.99) and especially the risk of lichen planus and OSCC (OR = 2.805 and 5.790, respectively). Similarly, the risk of oral disease was also more in the heterozygote (AG) than the common allele homozygote (AA) of TNF-ß (A252G) polymorphism (rs909253) (OR = 1.483). CONCLUSION: We conclude that the SNPs rs361525 and rs909253 were significantly associated with oral pre-cancer and OSCC.

An update on the diagnostic biomarkers for asthma.

Asthma is a respiratory disorder accounts for ~339 million cases per annum. The initial diagnosis of asthma relies on the symptomatic identification of characters, such as wheeze, shortness of breath, chest tightness, and cough. The presence of two or more of these symptoms may be considered as indicative of asthma. The asthma-diagnostic also involves spirometry test before and after inhaling a bronchodilator like albuterol. Because asthma pathophysiology involves participation of immune system, the cytokines play an important role. The review discusses various molecules that are or may be used as biomarkers for the asthma diagnosis.

Metals toxicity and its correlation with the gene expression in Alzheimer's disease.

Alzheimer's disease is a common neurodegenerative disease in the elderly population and a leading cause of dementia. Genetics and environmental risk factors were considered to play a major role in the onset of the disease. This study aimed to examine the correlation between different metals levels and the gene expression in Alzheimer's patients with age-matched control subjects. Non- essential metals were measured in the whole blood due to its higher concentration in red blood corpuscles (RBCs) and essential biometals in the serum samples of Alzheimer's disease (AD) by using Inductively coupled plasma optical emission spectroscopy (ICP-OES) that allows the analysis and detection of the different elements at low levels. Gene expression level was performed by quantitative real-time PCR (qRT-PCR). In this study, the levels of Lead and Arsenic metals were not detected in the AD patient samples. Cadmium, Mercury, and Aluminum were found higher in cases as compared to controls with 0.009240 ± 0.0007707 (P = < 0.0001), 0.02332 ± 0.001041 (P = < 0.0001), and 0.09222 ± 0.02804 (P = 0.0087) respectively. Essential biometal like copper was higher 0.1274 ± 0.02453 (P = 0.0254) in cases, while iron 0.1117 ± 0.009599 (P = 0.0304) and zinc 0.03800 ± 0.003462 mg/L were found significantly lower as compared to controls. All targeted genes such as APP, PSEN1, PSEN2, and APOE4 were found up-regulated in AD patients. We concluded that there was no significant correlation between metals dyshomeostasis and gene expressions in this study.

Serum vitamin D is a biomolecular biomarker for proliferative diabetic retinopathy.

BACKGROUND: Vitamin D is a multi-functional fat-soluble metabolite essential for a vast number of physiological processes. Non-classical functions are gaining attention because of the close association of vitamin D deficiency with diabetes, and its complications. The present study was undertaken to evaluate the role of vitamin D as a biomarker for proliferative diabetic retinopathy. METHODS: A tertiary care center based cross-sectional study was undertaken. Seventy-two consecutive cases of type 2 diabetes mellitus were included. Diagnosis of diabetes mellitus was made using American Diabetes Association guidelines. Study subjects included: diabetes mellitus with no retinopathy (No DR) (n = 24); non-proliferative diabetic retinopathy (n = 24); and proliferative diabetic retinopathy (n = 24) and healthy controls (n = 24). All of the study subjects underwent complete ophthalmological evaluation. Best Corrected Visual Acuity (BCVA) was measured on the logarithm of the minimum angle of resolution (logMAR) scale. Serum 25-OH Vitamin D assay was done using chemiluminescent microparticle immunoassay technology. Diagnostic accuracy of vitamin D was assessed using receiver operating characteristics curve analysis and area under curve (AUC) was determined for the first time. RESULTS: ANOVA revealed a significant decrease in serum vitamin D levels with severity of diabetic retinopathy (F = 8.95, p < 0.001). LogMAR BCVA was found to increase significantly with the severity of DR (F = 112.64, p < 0.001). On AUC analysis, a cut off value of 18.6 ng/mL for Vitamin D was found to be significantly associated with proliferative diabetic retinopathy [sensitivity = 86.36% (95% CI 65.1-96.9); specificity = 81.82% (95% CI 59.7-94.7); AUC = 0.91 (excellent); and Z value = 8.17]. CONCLUSIONS: Serum vitamin D levels of ≤ 18.6 ng/mL serve as sensitive and specific indicator for proliferative disease, among patients of DR.