Both aluminum and ethanol are pro-oxidants and neurotoxic. Considering the possibilities of co-exposure and sharing mechanisms of producing neurotoxicity, the present study was planned to identify the level of aluminum-induced oxidative stress in altered pro-oxidant (ethanol exposure) status of cerebrum. Male rats were coexposed to aluminum and ethanol for 4 weeks. After the exposure period, cerebral levels of protein, reduced glutathione (GSH), lipid peroxidation (TBARS) were measured. Activities of catalase, superoxide dismutase (SOD), glutathione reductase (GR) and glutathione perioxidase (GPx) of cerebrum were estimated. In most of the cases significant correlations were observed between the alterations and graded ethanol doses, suggesting a dose-dependency in pushing the oxidant equilibrium toward pro-oxidants. Aluminum is found to influence significantly all the studied parameters of oxidative stress. Likewise, ethanol also influenced these parameters significantly, except GR, while the interaction between ethanol and aluminum could significantly influence only the GSH content and GR activity of cerebrum. Present study demonstrate that coexposure of aluminum with pro-oxidant might favor development of aluminum-induced oxidative stress in cerebrum. This observation might be helpful in understanding of mechanism of neurodegenerative disorders and ameliorate them.

Diabetic nephropathy is a complication of diabetes mellitus. This present study investigates the status of copper and magnesium in diabetic nephropathy cases to establish a possible relation. Forty patients of diabetic nephropathy participated in the study as cases. Forty age- and sex-matched healthy individuals served as controls. Blood samples were collected from both cases and controls for determination of FBS, PPBS, HbA1c, microalbumin, copper, and magnesium levels. The mean concentrations of FBS, PPBS, HbA1c, and microalbumin of cases were significantly higher than that of controls. The mean magnesium levels of cases (1.60 ± 0.32 meq/L) were significantly lower than controls 2.14 ± 0.16 meq/L (p < 0.05). But the mean copper levels of cases, 165.42 ± 5.71 μg/dl, shows no significant difference with controls, 166.6 ± 5.48 μg/dl, (p > 0.05).The findings in the present study suggest that hypomagnesemia may be linked with development of diabetic nephropathy.

Background: Cardiac marker enzymes are measured to evaluate the heart function. The diagnosis of acute myocardial infarction can be achieved by electrocardiogram (ECG) changes and elevation of cardiac marker enzymes like creatine kinase, lactate dehydrogenase (LDH), aspartate transaminase (AST) and troponin I. Objective: To estimates the levels of AST and troponin I among patients of acute myocardial infarction, and to compare with those among health controls. Materials and Methods: This study was carried out among 50 cases of acute myocardial infarction and 50 age and sex matched healthy individuals. Serum samples of cases, collected after 5 hours and within 24 hours from the onset of chest pain and of controls were analyzed for AST by modified IFCC method and for troponin I by chemiluminescence-sandwich method. Results: The mean levels of AST and troponin I in cases and controls revealed that mean levels of AST and cardiac troponin I in cases (296.02±SD 135.69 IU/L and 57.34±SD 12.83 ng/ml, erspectively) are significantly higher than among controls (25.50±SD 6.22 IU/L and 0.31±SD 0.15 ng/ml, respectively). The differences between cases and controls are statistically significant (p<0.0001). Conclusion: The diagnostic efficiency of AST and troponin I were superior because they are specific to myocardial injury.

Abstract⎯Cerebellum is unique in restraining amyloid induced neurodegenerative changes. Amyloidosis and oxidant imbalance is common in aluminum exposure. Interestingly, aluminum itself does not pose any redox activity still it is associated with oxidant imbalance, and, it can aggravate the situation of already exist ing oxidant threat. Male rats were exposed to aluminum for 4 weeks along with exposure to 4 different doses of ethanol. After the treatment period, cerebellar level of protein, reduced glutathione (GSH), lipid perioxi dation (TBARS) were measured. Activities of catalase, superoxide dismutase (SOD), glutathione reductase (GR) and glutathione perioxidase (GPx) were also estimated from the homogenized cerebellar tissue. In the present regimen of aluminum exposure, the cerebellum has shown significant reduction only in GPx activity. However, when aluminum was coexposed with ethanol, it contributed significantly to increase the cerebellar oxidant imbalance by (a) compromising the GSH restoration system, (b) reducing enzymatic peroxide scav enging system of cerebellum, (c) restricting the capability to cope with oxidative stress, as well as (d) down grading the resistance to oxidative damage in response to chemical stress. Present study demonstrates that coexposure of aluminum with pro oxidant favored development of aluminum induced oxidative stress in cerebellum. These observations enlighten the role of pro oxidants in the process of oxidative degeneration of cerebellum. With further studies, the present observation can be useful to understand the mechanism of neu rodegenerative disorders and ways to ameliorate them.

The concurrent presence of oxidative stress (OS) and aluminium exposure is an inducer of neurodegenerative changes. Aluminium can augment OS in a pro-oxidant dominant condition. Antioxidative property of α-tocopherol may be useful in restricting these degenerative changes in the brain. OS parameters are tested in frontal cortex (FC), hippocampus (HC), and cerebellum (CL) of α-tocopherol-supplemented (5 IU/day) male Wistar rats exposed to aluminium (10 mg Al/Kg/day; "Al"), ethanol (0.6 g ethanol/Kg/day; "Et"), and both ("Al-Et") and vehicle-treated control ("C") for 4 weeks. The α-tocopherol supplementation restricted regional alterations of reduced glutathione, superoxide dismutase, catalase, and glutathione peroxidase. Accordingly, the regional superoxide and peroxide handling capacities (SPHC) also remain unaltered. Al-Et group demonstrated significant elevation in the lipid peroxidation level in FC and CL regions compared to the group C; similar elevations in lipid peroxidation were noted in all the tested brain regions of Al group. Likewise, declines in glutathione reductase activity were noted in HC (versus Et group) and CL (versus Al and Et groups) of Al-Et group. Interestingly, changes in behavioral patterns of all the treatment groups are comparable while differing from that of the control group. Significant difference with group C is observed during first through fourth weeks, third to fourth weeks, and second to third weeks in terms of spontaneous motor activity, Rota Rod performance, and Hebb-Williams maze performance, respectively. Hence, the current dose and duration of α-tocopherol supplementation failed to provide full protection against the aluminium-induced neurodegeneration; nevertheless, it could provide only partial protection toward aluminium-induced augmentation of OS in specific brain regions.