Protective effect of curcumin on cypermethrin-induced oxidative stress in Wistar rats

The aim of present study was to investigate the protective effect of curcumin on cypermethrin-induced changes in blood biochemical markers and tissue antioxidant enzyme in rats. Rats were divided into six groups of six each: group I used as control and II and III groups were used as vehicle control. While, groups IV, V and VI were orally treated with curcumin (100 mg/kg body weight), cypermethrin (25 mg/kg body weight) and cypermethrin plus curcumin, respectively for 28 days. Serum biochemical markers were measured in the serum, and the levels of lipid peroxidation and antioxidant enzyme activity were determined in the liver, kidney and brain. Cypermethrin administration caused elevated level of blood biochemical markers in serum and lipid peroxidation in liver, kidney and brain. While the activities of non-enzymatic and enzymatic antioxidants levels were decreased except superoxide dismutase in liver, kidney and brain tissues. The presence of curcumin with cypermethrin significantly decreased the blood biochemical markers and lipid peroxidation but significantly increased the reduced glutathione, catalase and glutathione peroxidase level and preserved the normal histological architecture of the liver, kidney and brain. Our results indicate that curcumin can be potent protective agent against cypermethrin-induced biochemical alterations and oxidative damage in rats.     

Lipid storage myopathies with unusual clinical manifestations

We describe the clinical presentation, course and pathologic findings found in three adult patients with lipid storage myopathy. Excessive lipid storage was found in Type 1 fibers of muscle. Clinical improvement on oral levo-carnitine therapy suggests the possibility of carnitine deficiency as the most likely etiology in two of the patients and one had mitochondrial myopathy confirmed on genetic analysis.     

Repeated preexposure or coexposure to arsenic differentially alters acetaminophen‐induced oxidative stress in rat kidney

Acetaminophen (AP) is a widely used, cheap, and over‐the‐counter nonsteroidal anti‐inflammatory drug. Its toxicity depends on the cytochrome P‐450 (CYP)‐mediated oxidation to the toxic metabolite N‐acetyl‐p‐benzoquinoneimine. On the other hand, arsenic, a global groundwater and environmental contaminant of major public health concern, decreases hepatic CYP content and its dependent monoxygenase activities. We hypothesized that arsenic exposure would reduce the AP toxicity. Our aim was to evaluate the effects of repeated preexposure or coexposure to arsenic on the oxidative stress induced by a single or repeated oral administration of AP in rat kidney and its possible relationship with the effects of arsenic on certain antioxidants. Rats were exposed to arsenic through drinking water at 25 ppm for 28 days. The dosages of AP used for a single administration after arsenic preexposure for 28 days were 420 and 1000 mg kg^?1, while for daily concurrent administration with arsenic for 28 days were 105 and 420 mg kg^?1 body weight. AP increased lipid peroxidation (LPO) in rat kidney where its acute administration caused more LPO than its subacute dosing. Repeated arsenic exposure differentially altered the AP‐induced LPO. Arsenic preexposure antagonized LPO induced by the acute AP administration; in contrast, arsenic coexposure aggravated the repeated dose (AP)‐mediated LPO. Arsenic‐mediated alterations in renal sensitivity to LPO did not appear to be linked to the antioxidants such as reduced glutathione, superoxide dismutase, catalase, glutathione peroxidase, and glutathione reductase; nor could it be related to glutathione‐S‐transferase activity. The results indicated that repeated arsenic preexposure decreased susceptibility of rat kidney to acute AP‐mediated oxidative stress; on the contrary, its coexposure rendered the rat kidney more vulnerable to oxidative stress induced by the repeated dosing of AP. © 2009 Wiley Periodicals, Inc. Environ Toxicol, 2011.     

A novel missense mutation C11994T in the mitochondrial ND4 gene as a cause of low sperm motility in the Indian subcontinent

We have analyzed the mitochondrial DNA of 34 oligoasthenozoospermic men along with 150 normozoospermic fertile men from the Indian subcontinent. A novel missense mutation (C11994T) in the ND4 gene, which replaces threonine with isoleucine, was observed in all of the oligoasthenozoospermic men but not in any of the normozoospermic fertile men.     

Impact of Sugar Factory Effluent on the Growth and Biochemical Characteristics of Terrestrial and Aquatic Plants

The physico-chemical characteristics of sugar industry effluent were measured and some were found to be above those limits permissible in the Indian irrigation water standard. A pot study was initially conducted to study the effects of different concentrations (20%, 40%, 60%, 80% and 100%) of sugar factory effluent on seed germination, seedling growth and biochemical characteristics of green gram and maize. A similar study was also carried out using the aquatic plants, water hyacinth and water lettuce. The higher effluent concentrations (above 60%) were found to affect plant growth, but diluted effluent (up to 60%) favored seedling growth.     

Influence of repeated preexposure to arsenic on acetaminophen-induced oxidative stress in liver of male rats

We evaluated whether repeated arsenic preexposure can increase acetaminophen-induced hepatic oxidative stress. Rats were exposed to arsenic (25 ppm; rat equivalent concentration of maximum groundwater contamination level) via drinking water for 28 days. Next day, they were given single oral administration of acetaminophen (420 or 1000 mg/kg b.w.). Hepatotoxicity was evaluated by assessing serum biomarkers, cytochrome-P450 (CYP) content, CYP3A4- and CYP2E1-dependent enzymes, lipid peroxidation and antioxidants. Arsenic or acetaminophen increased serum ALT and AST activities and depleted CYP. Arsenic decreased, but acetaminophen increased CYP-dependent enzyme activities. These agents independently increased lipid peroxidation and decreased antioxidants. Arsenic did not alter the effects of acetaminophen on serum biomarkers, caused further CYP depletion and decreased acetaminophen-mediated induction of drug-metabolizing enzymes. Arsenic enhanced the lower dose of acetaminophen-mediated lipid peroxidation and glutathione depletion with no further alterations in enzymatic antioxidants. However, arsenic attenuated the higher dose-mediated lipid peroxidation and glutathione depletion with improvement in glutathione peroxidase and glutathione reductase activities, further decrease in catalase and no alterations in superoxide dismutase and glutathione-S-transferase activities. Results show that arsenic preexposure increased the susceptibility of rats to hepatic oxidative stress induced by the lower dose of acetaminophen, but reduced the oxidative stress induced by the higher dose.     

Prevalence of diabetes mellitus in Indian tribal population: a systematic review and meta-analysis

International Journal of Diabetes in Developing Countries - Non-communicable diseases are the most serious public health threat of the twenty-first century. Diabetes is becoming a major public...     

Myrtenal alleviates hyperglycaemia,hyperlipidaemia and improves pancreatic insulin level in STZ-induced diabetic rats

Context: Myrtenal is monoterpene a constituent of essential oils found mainly in herbs such as mint, pepper, cumin, etc. It exerts admirable pharmacological activities against many diseases including diabetes. Hyperlipidaemia is a secondary complication of diabetes and also a major risk factor for cardiovascular diseases.

Objective: The present study investigated the possible antihyperlipidaemic efficacy of myrtenal on plasma glucose, pancreatic insulin, plasma and tissue lipid levels in streptozotocin (STZ) induced diabetic rats.

Materials and methods: Diabetes was induced in male Wistar rats by a single intraperitoneal injection of STZ (40?mg/kg b.w.). Myrtenal (80?mg/kg) was administered orally to diabetic rats for a period of 28 d. Plasma glucose, pancreatic insulin, TC, TGs, FFAs, PLs, LDL-C, HDL-C, VLDL, atherogenic index, (HMG-CoA) reductase, LPL, LCAT and liver histology were analyzed.

Results: Diabetic rats showed significantly (p?<?0.05) increased plasma glucose (273.18?mg/dL), total cholesterol (142?mg/dL), triglycerides (126?mg/dL), free fatty acids (118?mg/dL), phospholipids (153?mg/dL), low-density lipoprotein (88.07?mg/dL), very low-density lipoprotein (25.2?mg/dL), atherogenic index, whereas a decrease in the levels of pancreatic insulin (97.48?ng/mg) and high-density lipoprotein (29.12?mg/dL). In addition, the activity of 3-hydroxy 3-methylglutaryl coenzyme A (HMG-CoA) reductase (0.94 HMG-CoA ratio/(mevalonate) increased significantly in contrast to the activities of lipoprotein lipase (4.87 μmoles of glycerol liberated/h/L) and lecithin cholesterol acyltransferase (54.61 μmoles of cholesterol esterified/h/L) in diabetic rats. Treatment with myrtenal significantly (p?<?0.05) improved the levels of plasma glucose, pancreatic insulin and lipid profiles. Moreover, the histopathological analysis of liver was also in agreement with the biochemical findings.

Discussion and conclusions: The present study indicates that myrtenal possess antihyperglycaemic and antihyperlipidemic properties, and could potentially be a useful phytochemical in treating diabetes.     

Novel mitochondrial DNA mutations in a rare variety of hypertrophic cardiomyopathy

We report a rare case of a 65 year old male with mid left ventricular cavity obstruction which is an uncommon form of hypertrophic cardiomyopathy with cytogenetic analysis revealing novel mutations in mitochondrial nucleic acid.     

Contribution of muscle biopsy and genetics to the diagnosis of chronic progressive external opthalmoplegia of mitochondrial origin

Chronic progressive external opthalmoplegia (CPEO) is the most common phenotypic syndrome of the mitochondrial myopathies. Muscle biopsy, which provides important morphological clues for the diagnosis of mitochondrial disorders, is normal in approximately 25% of patients with CPEO, thus necessitating molecular genetic analysis for more accurate diagnosis. We aimed to study the utility of various histochemical stains in the diagnosis of CPEO on muscle biopsy and to correlate these results with genetic studies. Between May 2005 and November 2007 all 45 patients diagnosed with CPEO were included in the study (23 males; mean age at presentation, 35 years). Thirty-nine patients had CPEO only and six had CPEO plus; two had a positive family history but the remaining 39 patients had sporadic CPEO. Muscle biopsy samples were stained with hematoxylin and eosin, modified Gomori’s trichrome stain, succinic dehydrogenase (SDH), cytochrome C oxidase (COX) and combined COX-SDH. Ragged red fibers were seen in 27 biopsies; seven showed characteristics of neurogenic atrophy only, and 11 were normal. The abnormal fibers were best identified on COX-SDH stain. A complete mitochondrial genome was amplified in muscle and blood samples of all patients. Mutations were found in transfer RNA, ribosomal RNA, ND, CYTB, COX I, II and III genes. Mitochondrial gene mutations were found in ten of the 11 patients with a normal muscle biopsy. The genetic mutations were classified according to their significance. The observed muscle biopsy findings were correlated with genetic mutations noted. Histological studies should be combined with genetic studies for the definitive diagnosis of CPEO syndrome.