ABSTRACT
Background The cytochrome P-450 2J2 (CYP2J2) is known to be one of the major enzymes of epoxygenase pathway of arachidonic acid in extrahepatic tissues, which produces series of regioisomeric cis-epoxyeicosatrienoic acids (EETs) such as 5,6-, 8,9-, 11,12-, and 14,15-EETs. In the present study, we analyzed the impact of a genetic variant in CYP2J2 on coronary artery disease (CAD) in the Telangana region of Indian population. Material and methods The case–control study consisted of 100 CAD cases and 110 healthy controls. The deoxyribonucleic acid was extracted using the salting out method. Genotyping and gene expression was performed by polymerase chain reaction (PCR)-restriction fragment length polymorphism and real-time-PCR methods. Results In the present study, the percentage of smokers, alcoholics, hypertensive patients, and diabetics was high. Increase in fasting glucose, urea, creatinine, fasting triglycerides, total cholesterol (TC), low-density lipoprotein-cholesterol (LDL-C), total cholesterol/high-density lipoprotein (TC/HDL), LDL/HDL, homocysteine, and C-reactive protein levels were significantly higher in patients with CAD than in controls (p < 0.001). CYP2J2 G-50T was associated with CAD (p = 0.04). The mRNA expression of CYP2J2 showed altered gene expression in this study among CAD patients in comparison with control (p = 0.01). Conclusions A functionally relevant polymorphism of the CYP2J2 gene was independently associated with an increased risk of CAD.
ABSTRACT
This study reports the protective effects of selenium on fluoride induced alterations in the activities of pro-oxidative (xanthine oxidase (XOD), lipid peroxidation (LPO) free radical scavenging, (catalase, superoxide dismutase (SOD), glutathione-s-transferase (GST), glutathione peroxidase (GPX), glutathione reductase (GR), glutathione) and metabolic (glucose-6-phosphate dehydrogenase, alanine amino transferase (ALAT), aspartate aminotransferase (AAT), creatine phosphokinase (CPK), acid phosphatase (AP), alkaline phosphatase (ALP)] enzymes along with fluoride and selenium levels in brain of mice. Animals were divided into control, NaF treated group (20 mg kg-1 body wt.-1 intraperitonial) and Selenium+NaF treated group (sodium selenite, 5 mg of selenium / 0.2 ml distilled water kg-1 body wt.-1 day) and were maintained for 14 days on respective treatments. The decreased bodyweight (-11.35%) as well as organosomatic index (-15.1%) of brain in NaF group were recovered in treatment of selenium along with NaF. The increased accumulation of fluoride (32.1%) in brain observed in NaF treated group compared to control was diminished in selenium+NaF treated group. Selenium levels (3.03%) increased in selenium+NaF treated group in compared to decrement in NaF treatment. The SOD (-16.6%), Catalase (-21.5%), GST (-13.72%), GPX (-19.16%), GR (-44.97%) activities and Glutathione (-23%) content in NaF treated group were decreased significantly compared to controls, which were significantly (p<0.01) recovered in selenium+NaF group. Increased XOD (10.85%) and LPO (8.61%) levels observed in brain of NaF treated mice were reversed with selenium treatment. Glucose-6-phosphate dehydrogenase (-46.98%), ALAT (-10.44%), AAT (-10.21%), CPK (-27.98%) were decreased and alkaline phosphatase (10.6%), acid phosphatase (24.09%) increased in brain of mice after administration of NaF. All metabolic enzymes were significantly (p<0.01) reversed after administration of selenium to the NaF treated group. Thus, the adverse effects of NaF on oxidative and metabolic enzymes of brain were reversible with ameliorative action of selenium supplementation. As evident in this study, the antioxidative nature of selenium coupled with its reversal effect on metabolic enzymes in brain of mice treated with fluoride suggests its use as antidote agent against fluorosis.
ABSTRACT
This study reports the effects of low level developmental Pb exposure on specific brain regions like hippocampus, cerebellum and cerebral hemispheres of antioxidant enzyme activities. Wistar dams were exposed to 50 ppm, 100 ppm and 500 ppm of Pb acetate in drinking water during pregnancy and lactation (gestation day 6 through PND 21 (post natal day) and activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and glutathione reductase (GR) were determined in the hippocampus, cerebellum and cerebral hemispheres of pups during treatment period (PND 7, 14, and 21 days) and also during withdrawl period (PND 35, 45, 60 and 90 days). During treatment period, SOD activity significantly (p < 0.05) decreased in all regions of all the treated groups with maximum decrease in 500 ppm treated group of 21 days, while GSH-Px and GR activities increased with maximum increase in 21 days aged 500 ppm group. During withdrawl period, the activities of all enzymes were significantly (p < 0.05) reversed. Thus the perinatal exposure of dams to variable dosages of low level lead results in characteristic neurochemical alterations in rat brain regions due to impaired antioxidants function.