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We investigated the antioxidant preventive effect of betaine on isoprenaline-induced myocardial infarction in male albino rats. Isoprenaline induced myocardial infarction was manifested by a moderate elevation in the levels of diagnostic marker enzymes (alanine aminotransferase, aspartate aminotransferase, lactate dehydrogenase and creatine phosphokinase) and homocysteine in plasma of experimental rats. Significant rise in the level of lipid peroxidation with a concomitant decline in the levels of myocardial non-enzymic (reduced glutathione) and enzymic antioxidants (glutathione peroxidase, glutathione-S-transferase, catalase and superoxide dismutase) was also observed. Oral pretreatment with betaine significantly prevented isoprenaline-induced alterations in the levels of diagnostic marker enzymes and homocysteine in plasma of experimental groups of rats. It counteracted the isoprenaline-induced lipid peroxidation and maintained the myocardial antioxidant defense system at near normal. Histopathological observations also confirmed the protective effect of betaine against isoprenaline-induced myocardial infarction. The results of the present investigation indicate that the protective effect of betaine is probably related to its ability to strengthen the myocardial membrane by its membrane stabilizing action or to a counteraction of free radicals by its antioxidant property.

The analgesic and anti-inflammatory properties of liver oils of four different sharks, namely Neohariotta raleighana, Centrosymnus crepidater, Apristurus indicus and Centrophorus scalpratus, captured from the Arabian Sea and the Indian Ocean were evaluated. While the analgesic property was determined using the acetic acid-induced mouse writhings and hot-plate reaction time, the anti-inflammatory activity was evaluated using the formalin-induced rat-paw edema. The oils examined were found to possess significant (P < 0.05) analgesic activity against acetic acid-induced writh- ings and hot-plate reaction in mice. In the formalin-induced edema, a sig- nificant (P < 0.05) inhibition of inflammation was observed between the 2nd and 4th hour showing 58-65% inhibition. These results suggest that liver oils of sharks from Indian waters are effective as analgesic and anti- inflammatory agents. The role of lipid components (squalene, alkylglycerols and polyunsaturated fatty acids) on anti-inflammatory and antinociceptive properties is highlighted. Inhibition of the synthesis of prostaglandins and other inflammatory mediators which probably account for the properties is discussed.

Physicochemical characteristics of proteins extracted from muscles excised from four distinct regions of mackerel were examined. Three regions were identified based on their fin position; namely anterior muscle, median muscle, posterior muscle and red muscles from beneath the lateral line. The biochemical characteristics like reactive sulphydryl groups, surface hydrophobicity, Ca2+ ATPase activity, turbidity, proximate composition and the functional characteristics such as viscosity, emulsion activity index (EAI) and emulsion stability (ES) were studied in the samples, from different regions. Sarcoplasmic protein (SPP) solubility was found to be higher in red muscles compared to that of white muscles, whereas myofibrillar protein (MFP) solubility was higher in white muscles particularly in the posterior portion. The MFP from posterior white muscles showed better viscosity, surface hydrophobicity and Ca2+ ATPase activity, which in turn contributed to the higher EAI and ES of this muscle portion. Variations in composition, electrophoretic pattern of proteins and selected functional properties (EAI) were noticed between red and white muscles, which may be of significance from the utilization point of the fish.

Tiger prawns (Penaeus monodon) were infected with white spot virus artificially by intramuscular injection of the virus inoculum. Haemolymph, hepatopancreas and muscle samples from the infected prawns were analyzed for glucose and enzymes viz aldolase, glucose-6-phosphatase, fructose-1,6-diphosphatase and glucose-6-phosphate dehydrogenase in the carbohydrate metabolism. Glucose content reduced to 33% of its original value in 24 h of infection and to 31% in 48 h. Almost 95% loss in activity was observed in the case of fructose 1,6-diphosphatase in hepatopancreas, whereas the reduction in activity in muscle was 67%, after 48 h of infection. Glucose-6-phosphatase showed a reduction of 16 and 13% in hepatopancreas and muscle respectively during 24 h of infection. The activity of glucose-6-phosphate dehydrogenase increased by 300% of original value in hepatopancreas, while in muscle the increase was only 30% of original value during 24 h of infection. No significant change in activity was noted in the case of aldolase. Even at moribund stage, the glycolytic pathway was not affected, as evident from the normal activity of aldolase observed in the present study.

Mullet ( Mugil cephalus ) muscle homogenates were adjusted to different pH ranging from 2 to12 and the proteins extracted were evaluated for changes in solubility and conformational characteristics viz. surface hydrophobicity and reactive sulphydryl groups. Altering the pH of muscle homogenate to acidic or alkaline increased protein solubility. The hydrophobicity of the proteins increased on exposure to extreme pH indicating unfolding. The reactive sulphydryl groups decreased at acidic and alkaline pH with the lowest at pH 4. When the pH of the muscle homogenates was brought back to the original pH (6.3), the protein solubility was found to decrease. Reactive sulphydryl groups and ANS hydrophobicity of the proteins increased on readjusting the pH resulting in a molten-globule state. The electrophortogram of the samples corresponded well with the observations. Alterations in functional properties of these modified proteins are an area of interest for commercial application.

Background: Helicobacter pylori is the major causative factor of ulcer but the use of ibuprofen and other non-steroidal anti-inflammatory drugs have also been implicated in development of ulcer. The purpose of the present study was to determine the anti-ulcer effect of glucosamine. Methods: The protective effect of glucosamine on ibuprofen-induced peptic ulcer in male albino rats was studied with respect to changes in the volume of gastric juice, acid output, pepsin activity, activities of membrane bound ATPases, protein content, glycoprotein components and histopathology. Results: Oral administration of ibuprofen caused significant increase in the number of lesions in the gastric mucosa, increases in the volume of gastric juice and acidity, and decreased activity of pepsin. The levels of protein content and glycoprotein components (hexose, hexosamine and sialic acid) and ATPase activities were also observed. Oral pretreatment with glucosamine resulted in significant reduction in the number of lesions in the gastric mucosa and decreases in the volume of gastric juice and acidity. The pepsin activity was also maintained at near normalcy. Prior oral administration of glucosamine significantly prevented the ibuprofen-induced depletion of protein and glycoprotein components and maintained the activities of membrane bound ATPases as compared to untreated ulcer induced group of rats. Conclusion: The anti-ulcerogenic activity of glucosamine might be ascribable to its ability to neutralize the hydrochloric acid secreted into the stomach and to its capability to strengthen the mucosal barrier by increasing mucosal glycoprotein synthesis and to its free radical scavenging property. Histopathological investigations of the mucosal tissue also support the anti-ulcerogenic effect of glucosamine.

The protective effect of PUFA concentrate prepared from fish oil on isoproterenol-induced myocardial infarction in male albino rats was investigated with respect to changes in the levels of diagnostic marker enzymes, cholesterol, triglycerides, free fatty acids, phospholipids, reduced glutathione (GSH) and lipid peroxides (LPO). Administration of PUFA concentrate significantly prevented the isoproterenol-induced elevation in the levels of plasma diagnostic marker enzymes (ALT [93.5%], AST [95.6%], LDH [94.7%] and CPK [96.1%]). PUFA concentrate feeding exerted a significant antilipidemic effect against isoproterenol-induced myocardial infarction by reducing the levels of lipid components in plasma (cholesterol [71.5%], triglycerides [79.7%] and free fatty acids [70.7%] and heart tissue (cholesterol [81.4%], triglycerides [76.3%] and free fatty acids [78.6%]). A tendency to prevent the isoproterenol-induced phospholipids depletion (74.4%) in the myocardium of experimental rats was also observed. The level of lipid peroxidation was also found to be significantly lower in PUFA treated animals (2.72+/-0.15nmol/ml in plasma; 1.18+/-0.08nmol/mg protein in heart tissue) as compared to that of isoproterenol-injected groups (5.77+/-0.43nmol/ml in plasma; 2.14+/-0.15nmol/mg protein in heart tissue) of rats. Also the level of reduced GSH significantly higher in the heart tissue of PUFA administered experimental rats (5.65+/-0.98 microg/g) as compared to myocardial infarction induced control rats (2.39+/-0.18 microg/g). The results of the present study indicate that the overall cardioprotective effect of PUFA concentrate is probably related to its ability to inhibit lipid accumulation by its hypolipidaemic property.

The present study was designed to examine the cardioprotective effect of betaine on mitochondrial function in isoprenaline-induced myocardial infarction in rats with respect to changes in the mitochondrial energy status and antioxidant defense system. Prior oral treatment with betaine significantly prevented the isoprenaline-induced elevation in the levels of diagnostic maker enzymes [alanine aminotransferase (ALT), aspartate aminotransferase (AST), lactate dehydrogenase (LDH), and creatine phosphokinase (CPK)] and homocysteine in plasma of the experimental group of rats. Its administration significantly counteracted the isoprenaline-induced aberrations in the myocardial energy status by maintaining the levels of myocardial ATP and betaine contents and the activities of mitochondrial TCA cycle enzymes [isocitrate dehydrogenase (ICDH), α-ketoglutarate dehydrogenase (α-KDH), succinate dehydrogenase (SDH), and malate dehydrogenase (MDH)] and respiratory marker enzymes (NADH dehydrogenase and cytochrome-c-oxidase) at near normalcy. It also exerted an antioxidant effect against isoprenalineinduced myocardial infarction by blocking the induction of mitochondrial lipid peroxidation (LPO). A tendency to minimize the isoprenaline-induced alterations in the level of reduced glutathione (GSH) and in the activities of glutathione-dependent antioxidant enzymes [glutathione peroxidase (GPx) and glutathione-S-transferase (GST)] and antiperoxidative enzymes [superoxide dismutase (SOD) and catalase (CAT)] in the heart mitochondria was also observed. The results of the present study indicate that the overall cardioprotective effect of betaine is probabl yr elated to its ability to maintain the myocardial energy status (ATP) at higher level by maintaining the activities of TCA cycle enzymes and respiratory marker enzymes at near normalcy, and/or to its free radical-scavenging ability against isoprenaline-induced lipid peroxidation, which is primarily responsible for the irreversible necrosis of the myocardial membrane.

We have investigated the preventive effects of squalene against isoprenaline-induced myocardial infarction in male albino rats. Supplementation with squalene significantly prevented the isoprenaline-induced adverse changes in the levels of protein and glycoprotein components in plasma and heart tissue of experimental groups of rats. It exerted an antioxidant effect by inhibiting the isoprenaline-induced lipid peroxidation and by maintaining the level of non-enzymatic free radical-scavenger, reduced glutathione at near normalcy. Histopathological observations also confirmed the possible cardioprotective action of squalene by maintaining the normal architecture of the heart tissue. The results of the present investigation demonstrate that supplementation with squalene offers cardioprotection in experimental rats by its antioxidant and membrane- stabilizing properties.

Oxidative stress is one of the mechanisms with a central role involved in the pathogenesis of myocardial infarction. The protective effect of glutamine on myocardial antioxidant defense system was investigated during isoprenaline-induced myocardial infarction, an animal model of myocardial infarction of human beings. Levels of diagnostic marker enzymes in plasma, reduced glutathione (GSH) and lipid peroxides and the activities of glutathione peroxidase, glutathione-S-transferase, catalase and superoxide dismutase in heart tissue were determined. Injection of isoprenaline caused significant increases in the levels of diagnostic marker enzymes in plasma and lipid peroxidation in heart tissue. A parallel decline in the levels of ATP (Adenosine triphosphate) and GSH and the activities of glutathione-dependent antioxidant enzymes and antiperoxidative enzymes in heart tissue was also observed. Prior oral administration of glutamine significantly prevented isoprenaline-induced adverse effects and maintained myocardial antioxidant status at near normal status. The cardioprotective effect of glutamine is probably related to a strengthening of the myocardial membrane by its membrane stabilizing action, or to a counteraction of free radicals by its antioxidant property, or to its ability to maintain near to normal status the activities of free radical scavenging enzymes and the level of GSH, which protect myocardial membrane against oxidative damage by decreasing lipid peroxidation.

The micronutrients (vitamins and minerals) are required in small amounts but are essential for health, development, and growth. Micronutrient deficiencies, which affect over two billion people around the globe, are the leading cause of many ailments including mental retardation, preventable blindness, and death during childbirth. Fish is an important dietary source of micronutrients and plays important role in human nutrition. In the present investigation, micronutrient composition of 35 food fishes (includes both finfishes and shellfishes) was investigated from varying aquatic habitats. Macrominerals (Na, K, Ca, Mg) and trace elements (Fe, Cu, Zn, Mn, Se) were determined by either atomic absorption spectroscopy (AAS) or inductively coupled plasma mass spectrometry (ICP-MS)/atomic emission spectrometry (ICP-AES). Phosphorus content was determined either spectrophotometrically or by ICP-AES. Fat-soluble vitamins (A, D, E, K) were analyzed by high-performance liquid chromatography (HPLC). The analysis showed that, in general, the marine fishes were rich in sodium and potassium; small indigenous fishes (SIFs) in calcium, iron, and manganese; coldwater fishes in selenium; and the brackishwater fishes in phosphorous. The marine fishes Sardinella longiceps and Epinephelus spp. and the SIFs were rich in all fat-soluble vitamins. All these recommendations were made according to the potential contribution (daily value %) of the species to the recommended daily allowance (RDA). Information on the micronutrients generated would enhance the utility of fish in both community and clinical nutrition.

Myocardial infarction is one of the major public concerns in both developed and developing countries. Recently, there is growing interest in potential healthcare applications of marine natural products in the field of cardiovascular research. In the present study, we have examined the membrane-stabilizing potential of marine mucopolysaccharide-chitosan in modulating the aberrations of thiol-dependent membrane-bound ATPases activities, mineral status, and cardiac diagnostic markers in isoproterenol-induced myocardial infarction condition in rats. Dietary intake of chitosan significantly (p

Fish collected from five different locations from the Calicut region, India were analysed for the levels of organochlorine pesticides (OCPs) and heavy metal (HM) residues in order to elucidate the status of these chemical contaminants in fish and shellfish meant for human consumption. The highest concentrations of OCPs detected in the edible portion of fish were 10.47, 70.57 and 28.35 ng g −1 wet weight, in marine, brackish water and freshwater, respectively. BHC and heptachlor epoxide formed the major share of OCPs in the marine fish while BHCs contributed to the major share in the freshwater and brackish water fish. The DDT (sum of DDT and its metabolites) ranged from 0.05 to 8 ng g −1 in the samples irrespective of the habitat. Among the HMs, Cu, Zn, Mn and Cr were present in the samples irrespective of the place of collection. About 22% of the samples from the freshwater area contained marginally higher lead content above the legal limit of 0.2–0.4 μg g −1 . The Cr content ranged from 0.1 to 1.1 μg g −1 in the fish with marginally higher content in the fish from freshwater and marine regions (0.55–1.1 μg g −1 ). Mercury was detected in the samples (55%) from marine habitat only. The concentrations of OCPs and HMs in the samples, in general, were below the maximum residual level recommended by various organizations.

We have studied the protective effect of chitosan on isoniazid- and rifampicin-induced hepatotoxicity with respect to the changes in the levels of diagnostic marker enzymes (in serum), lipid components and lipid peroxidation (in serum and liver). The oral administration of antitubercular drugs caused a significant elevation in the levels of diagnostic marker enzymes and cholesterol, triglycerides, free fatty acids and lipid peroxidation in serum and liver of experimental rats. There was a slight decline in the level of phospholipids in liver tissue also observed. Co-administration of chitosan significantly prevented the antitubercular drugs-induced elevation in the levels of serum diagnostic marker enzymes (alanine amino transferase, aspartate amino transferase, lactate dehydrogenase, acid phosphatase and alkaline phosphatase) in experimental groups of rats. It exerted a significant antilipidemic effect against isoniazid- and rifampicin-induced hepatitis by maintaining the levels cholesterol, triglycerides, free fatty acids and phospholipids in serum and liver at near normalcy. A tendency to prevent the isoniazid- and rifampicin-induced lipid peroxidation was also observed. The results of the present study indicated that the hepatoprotective effect of chitosan might be ascribable to its antilipidemic effect and/or antioxidant property.

We have examined the protective effect of taurine on the myocardial antioxidant defense system in isoprenaline (isoproterenol)-induced myocardial infarction in rats, an animal model of myocardial infarction in man. Levels of diagnostic marker enzymes in plasma, lipid peroxides and reduced glutathione, and the activity of glutathione-dependent antioxidant enzymes and antiperoxidative enzymes in the heart tissue were determined. Intraperitoneal administration of taurine significantly prevented the isoprenaline-induced increases in the levels of alanine aminotransferase, aspartate aminotransferase, lactate dehydrogenase, and creatine phosphokinase in the plasma of rats. Taurine exerted an antioxidant effect against isoprenaline-induced myocardial infarction by preventing the accumulation of lipid peroxides and by maintaining the level of reduced glutathione and the activity of glutathione peroxidase, glutathione-S-transferase, catalase and superoxide dismutase at near normality. The results indicated that the cardioprotective potential of taurine was probably due to the increase of the activity of the free radical enzymes, or to a counteraction of free radicals by its antioxidant nature, or to a strengthening of myocardial membrane by its membrane stabilizing property.

The present study examined the antiulcer effect of glucosamine on mucosal antioxidant defense system in ibuprofen-induced peptic ulcer in male albino rats. The number of lesions in the gastric mucosa, volume of gastric juice, acid output, pepsin activity, lipid peroxides, reduced glutathione content and the activities of glutathione dependent antioxidant enzymes (glutathione peroxidase and glutathione-S-transferase) and antiperoxidative enzymes (catalase and superoxide dismutase) were determined. Prior oral administration of glucosamine significantly prevented the ibuprofen-induced increases in the number of lesions in the gastric mucosa, volume of gastric juice and acidity. It also maintained the activity of pepsin at near normal level. Oral pretreatment of glucosamine exerted a significant antioxidant effect by preventing ibuprofen-induced lipid peroxidation and by maintaining the level of reduced glutathione and the activities of mucosal antioxidant enzymes at near normalcy. The results of the present investigation indicate that the antiulcer activity of glucosamine is related to its ability to neutralize the hydrochloric acid secreted into the stomach and to its antioxidant capability to inhibit ibuprofen-induced lipid peroxidation.

The protective effect of squalene on membrane function and mineral status was examined in isoproterenol-induced myocardial infarction in male albino rats. The pretreatment with squalene at 2% level along with feed significantly reduced the isoproterenol-induced rise in the levels of plasma diagnostic marker enzymes (ALT, AST, LDH and CPK). It counteracted isoproterenol-induced lipid peroxidation in plasma and heart tissue, and maintained the level of reduced glutathione in the heart tissue at near normalcy. Supplementation of squalene also exerted membrane stabilizing action against isoproterenol-induced myocardial infarction by maintaining the activities of membrane-bound ATPases (Na+, K+ ATPase and Ca2+ ATPase) in heart tissue and the mineral status (sodium, potassium and calcium) in plasma and heart tissue at near normal levels. The cardioprotective effect of squalene might be ascribable to its antioxidant nature and membrane stabilizing property.

This study was designed to examine the effects of squalene on tissue antioxidant status in isoproterenol-induced myocardial infarction in male albino rats. Levels of diagnostic marker enzymes [alanine aminotransferase (ALT), aspartate aminotransferase (AST), lactate dehydrogenase (LDH), and creatine phosphokinase (CPK)] in plasma, lipid peroxides, reduced glutathione, and the activities of glutathione-dependent antioxidant enzymes [glutathione peroxidase (GPx) and glutathione-S-transferase (GST)] and antiperoxidative enzymes [catalase (CAT) and superoxide dismutase (SOD)] in the heart tissue of experimental groups of rats were determined. The prior administration of squalene at 2% level along with feed for 45 days significantly prevented the isoproterenol-induced elevation in the levels of diagnostic marker enzymes in plasma of experimental rats. Squalene also exerted an antioxidant effect against isoproterenol-induced myocardial infarction by blocking the induction of lipid peroxidation. A tendency to prevent the isoproterenol-induced alterations in the level of reduced glutathione and in the activities of glutathione-dependent antioxidant enzymes and antiperoxidative enzymes was also observed. The cardioprotective effect of squalene might be ascribable to its antioxidant property and membrane stabilizing action.

Oral treatment with the ethanol extract of Hemidesmus indicus roots (100 mg/kg, for 15 days) significantly prevented rifampicin and isoniazid-induced hepatotoxicity in rats.

The effect of pre-treatment with an alcoholic extract of Picrorhiza kurroa, a herbal drug, on D-galactosamine-induced hepatitis in rats was investigated with respect to the activities of serum marker enzymes, glycolytic enzymes, gluconeogenic enzymes, glucose-6-phosphate dehydrogenase, and membrane-bound ATPases and the levels of lipid peroxides and hepatic thiols. Prior oral treatment with P. kurroa extract significantly prevented the D-galactosamine-induced increases in the activities of serum marker enzymes, glycolytic enzymes, glycogen phosphorylase, and glucose-6-phosphate dehydrogenase and the decreases in the activities of key gluconeogenic enzymes and membrane-bound ATPases in the liver. The extract also exerted an antioxidant effect against D-galactosamine-induced hepatitis by blocking the induction of lipid peroxidation and by preventing the depletion of hepatic thiols. The present findings confirm that P. kurroa is hepatoprotective in experimentally induced hepatitis in rats.

Oral pre-treatment with alcoholic extract of Picrorrhiza kurroa rhizomes and roots (50 mg/kg/day for 10 days) significantly prevented the d -galactosamine-induced alterations in respiration and oxidative phosphorylation of liver mitochondria.

The antiulcerogenic effects of the ethanol extract of Picrorrhiza kurroa rhizomes and roots (PK) on HCl/ethanol-induced ulceration in rats with respect to acid/pepsin, lipid peroxidation, antioxidant status, proteins and glycoproteins in the gastric mucosa have been investigated. Oral pre-treatment with PK (100 mg/kg/day for 10 days) significantly prevented the induced ulceration and maintained the rats at near normal status.

In d -galactosamine-induced hepatitis in rats, a significant increase of lipid peroxidation and a decrease in liver antioxidant enzymes levels are observed. Pretreatment with the ethanol extract of Picrorrhiza kurroa prevented these alterations.

The present study examined the preventive effects of Picrorhiza kurroa, an ayurvedic medicinal plant, on D-galactosamineinduced hepatitis in rats, an animal model of both drug-induced hepatitis and viral hepatitis of human beings. Levels of protein, glycoprotein, cholesterol, phospholipids, and lipid peroxide products in plasma and erythrocyte membrane and the activities of erythrocyte membrane antiper-oxidative enzymes superoxide dismutase and catalase were determined. Prior oral treatment with an alcoholic extract of Picrorhiza kurroa significantly prevented the D-galactosamine-induced decreases in the levels of protein and glycoprotein and in the activities of superoxide dismutase and catalase. A tendency to prevent the D-galactosamine-induced alterations in the levels of cholesterol, phospholipids and lipid peroxides was also observed. The antihepatotoxic potential of Picrorhiza kurroa might be ascribable to the antioxidant and hypolipidemic nature of Picrorhiza kurroa.

Myocardial infarction is a major public health concern and the leading cause of death all over the world. A better understanding of the processes involved in myocardial infarction has stimulated the search for biomolecules, which could limit the myocardial injury. We determined the protective activity of L-glutamine on mitochondrial function in isoprenaline-induced myocardial infarction in rats, an animal model of myocardial infarction in man. Oral pre-treatment with glutamine significantly inhibited the isoprenaline-induced changes in the levels of troponin T and homocysteine in the plasma. It conserved the activities of tricarboxylic acid cycle enzymes (isocitrate dehydrogenase, α-ketoglutarate dehydrogenase, succinate dehydrogenase, malate dehydrogenase) and respiratory marker enzyme (NADH dehydrogenase) and the level of myocardial ATP content at levels comparable to that of normal controls. It also attenuated isoprenaline-induced oxidative stress in rat mitochondria and preserved the antioxidant defence system at near normal. The results indicate that the cardioprotective effect of glutamine can be correlated directly with its ability to activate the energy status and antioxidant defence system. Keywords: isoprenaline

Despite considerable advances in diagnosis and management over the last three decades, acute myocardial infarction continues to be a major public health problem. It is predicted that ischemic heart diseases will constitute the major disease-burden worldwide in the year 2020. In the present study, an attempt has been made to examine the effects of dietary chitosan supplementation on lipid peroxidation and cardiac antioxidant defense system in isoprenaline-induced myocardial infarction in rats, an animal model of myocardial infarction in man. Dietary chitosan intake significantly attenuated the isoprenaline-induced lipid peroxidation and maintained the level of reduced glutathione at near normal. Its administration demonstrated an antioxidant effect by maintaining the activities of myocardial glutathione dependent antioxidant enzymes (glutathione peroxidase and glutathione-S-transferase) and antiperoxidative enzymes (superoxide dismutase and catalase) at levels comparable to that of controls. The results of the present study indicate that the salubrious effects of dietary supplementation of chitosan is probably related to a counteraction of free radicals and/or to normal maintenance of the activities of free radical enzymes and the level of GSH, which protect myocardial membrane against oxidative damage by decreasing lipid peroxidation.

Stress can be defined as physical and psychological modifications that disrupt the homeostasis and the balance of organisms. Stress is known as one of the most important reasons of several diseases. In the present study, the anti-stress effect of betaine was evaluated with reference to its antioxidant property. Wistar albino rats were divided into four groups such as control, betaine, restraint stress (6 h/day for 30 days), and betaine + restraint stress. The oxidative damage was assessed by measuring the protein and corticosterone in plasma, lipid peroxidation, non-enzymic (reduced glutathione), and enzymic antioxidants (glutathione peroxidase, glutathione-S-transferase, catalase, and superoxide dismutase) in the lymphoid organs of thymus and spleen. Followed by the induction of restraint stress, the non-enzymic and enzymic antioxidants were significantly decreased with concomitant increase observed in the levels of corticosterone and lipid peroxidation. Oral pretreatment with betaine (250 mg/kg body weight daily for a period of 30 days) significantly (P < 0.001) prevented the restraint stress-induced alterations in the levels of protein and corticosterone in plasma of experimental groups of rats. It counteracted the restraint stress-induced lipid peroxidation and maintained the antioxidant defense system in the lymphoid tissues at near normal. The findings suggest that betaine possesses significant anti-stress activity, which may be due to its antioxidant property.

Chemoprevention by medicinal plants has evolved as a practical strategy to control the incidence of cancer. Azadirachta indica (neem) containing various bioactive components is a promising candidate for chemoprevention. The present study was undertaken to evaluate the chemopreventive efficacy of the bioactive subfractions ethyl acetate chloroform insoluble fraction (ECIF) and the methanol ethyl acetate insoluble fraction (MEIF) following activity-guided fractionation of neem leaf extract. Analysis of the mechanism of chemoprevention revealed multitargeted mode of action that involved modulation of xenobiotic-metabolizing enzymes, inhibition of cell proliferation, induction of mitochondrial apoptosis, and abrogation of NF-κB signaling. HP-TLC, GC-MS and LC-MS analyses indicated the presence of several polar phytochemical entities in the neem leaf subfractions that might be responsible for their potent chemopreventive efficacy.

We have studied the synergistic effects of squalene and polyunsaturated fatty acids (PUFA concentrate) on isoprenaline-induced infarction in rats with respect to changes in the levels of plasma diagnostic marker enzymes and myocardial antioxidant defense system. Intraperitoneal injection of isoprenaline caused a significant elevation in the levels of diagnostic marker enzymes; alanineaminotranferase (ALT), aspartate aminotransferase (AST), lactate dehydrogenase (LDH) and creatine phosphokinase (CPK) in plasma of experimental rats. There was a significant rise in the level of lipidperoxidation with concomitant decline in the level of reduced glutathione (GSH) and in the activities of glutathione-dependent antioxidant enzymes; glutathione peroxidase (GPX) and glutathione-Stransferase (GST), and antiperoxidative enzymes; superoxide dismutase (SOD) and catalase (CAT) in heart tissue. Combined supplementation of squalene and PUFA concentrate significantly prevented the isoprenaline-induced elevations in the levels of diagnostic marker enzymes in plasma of experimental groups of rats. A tendency to counteract the isoprenaline induced lipid peroxidation was also noticed. Their combined administration maintained the level of GSH and the activities of glutathione-dependent antioxidant enzymes and antiperoxidative enzymes at near normalcy. The results of the present study indicated that the combined administration of squalene and PUFA concentrate exerted significantly better cardio-protection against isoprenaline-intoxication as compared to that of per secondsupplementation.

We evaluated the protective effects of subfractions of the ethyl acetate fraction (EAF) and the methanolic fraction (MF) from the crude ethanolic extract (CEE) of Azadirachta indica A. Juss (neem) leaves against various free radicals and hydrogen peroxide (H 2 O 2 )-induced oxidative damage to red blood cells (RBCs) and pBR322 DNA. Neem leaf fractions reduced DPPH * , ABTS ++ , superoxide (O ·― ), hydroxyl (OH'), and nitric oxide radicals to nonradical forms in a concentration-dependent manner. Treatment with the benzene insoluble fraction from EAF (EBIF), the chloroform insoluble fraction from EAF (ECIF), the chloroform insoluble fraction from MF (MCIF), and the ethyl acetate insoluble fraction from MF (MEIF) significantly mitigated H 2 O 2 -induced oxidative damage to RBCs and pBR322 DNA. Although we found low in vitro free radical scavenging activity for the benzene insoluble fraction from EAF (EBSF), the chloroform soluble fraction from EAF (ECSF), the chloroform soluble fraction from MF (MCSF), and the ethyl acetate soluble fraction from MF (MESF), these fractions showed no effect on H 2 O 2 -induced lipid peroxidation and pBR322 DNA damage. High-performance liquid chromatography (HPLC) and TLC-latroscan analysis revealed that the greater efficacy of EBIF, ECIF, MCIF, and MEIF may be due to the presence of more polar compounds such as nimbolide and quercetin. Our studies suggest that the antioxidant and protective effects of active neem leaf fractions against H 2 O 2 -induced lipid peroxidation and pBR322 DNA damage can be attributed to their ability to inhibit various free radicals.

We evaluated the chemopreventive potential of the ethyl acetate fraction (EAF) and methanolic fraction (MF) of Azadirachta indica (neem) leaf on 7,12-dimethylbenz[a]anthracene (DMBA)-induced rat mammary carcinogenesis. Estradiol and estrogen receptor status, xenobiotic-metabolizing enzyme activities, redox status, DNA and protein modifications, and the expression of cell proliferation, and apoptosis related proteins in the mammary gland and liver were used as biomarkers of chemoprevention. Administration of both EAF and MF at a dose of 10 mg/kg bw effectively suppressed tumour incidence. Chemoprevention by neem leaf fractions was associated with modulation of hormone and receptor status, xenobiotic-metabolising enzymes, and lipid and protein oxidation, with upregulation of antioxidants, inhibition of oxidative DNA damage, protein modification, and cell proliferation, and induction of apoptosis. However EAF rich in constituent phytochemicals was more effective than MF in modulating multiple molecular targets. These results provide evidence for the chemopreventive efficacy of neem leaf fractions in the rat mammary tumour model.

Cardiovascular diseases are emerging as a major public health problem in most parts of the world even in developing countries still afflicted by infectious diseases, undernutrition, and other illnesses related to poverty. In the present study, we investigated the protective effect of betaine, a potent lipotropic molecule, on changes in the levels of membrane-bound ATPase activities, lipid peroxidation, sulfhydryl activities, and mineral status in isoprenaline-induced myocardial infarction in Wistar rats, an animal model of myocardial infarction in man. Oral administration of betaine (250 mg/kg body weight/day for a period of 30 days) significantly (p < 0.05) reduced the isoprenaline-induced abnormalities noted in the levels of sodium, potassium, and calcium in plasma and heart tissue. Pretreatment with betaine significantly attenuated isoprenaline-induced membrane-bound ATPase depletion in the heart tissue and preserved the myocardial membrane-bound ATPase activities at levels comparable to that of control rats. Oral administration of betaine significantly attenuated the isoprenaline-altered sulfhydryl groups in the heart tissue and preserved the myocardial sulfhydryl activities at levels comparable to that of control rats. It also significantly counteracted the isoprenaline-mediated lipid peroxidation and maintained the level at near normal. In the results of the present study, betaine administration significantly prevented the isoprenaline-induced alterations in the activities of membrane-bound ATPases, lipid peroxides, myocardial sulfhydryl levels, and maintained the mineral status at near normal.

Mitochondria are an important intracellular source and target of reactive oxygen species. The life span of a species is thought to be determined, in part, by the rate of mitochondrial damage inflicted by oxygen free radicals during the course of normal cellular metabolism. In the present study, we have investigated the protective effect of squalene supplementation for 15 days and 30 days on energy status and antioxidant defense system in liver mitochondria of 18 young and 18 aged rats. The dietary supplementation of 2% squalene significantly minimized aging associated alterations in mitochondrial energy status by maintaining the activities of TCA cycle enzymes (isocitrate dehydrogenase, alpha-ketoglutarate dehydrogenase, succinate dehydrogenase and malate dehydrogenase) and respiratory marker enzymes (NADH dehydrogenase and cytochrome-c-oxidase) at higher level in the liver mitochondria of aged rats compared with unsupplemented controls. It exerted an antioxidant effect by inhibiting mitochondrial lipid peroxidation (malondialdehyde) in liver of young and aged rats. Supplementation with squalene also maintained the mitochondrial antioxidant defense system at higher rate by increasing the level of reduced glutathione and the activities of glutathione-dependent antioxidant enzymes (glutathione peroxidase and glutathione-S-transferase) and antiperoxidative enzymes (superoxide dismutase and catalase) in the liver of young and aged rats. The results of this study provide evidence that dietary supplementation with squalene can improve liver mitochondrial function during aging and minimize the age-associated disorders in which reactive oxygen species are a major cause.

Tuberculosis is a dangerous disease and its death toll is increasing year by year. Intake of isoniazid and rifampicin, the most common antitubercular drugs, lead to fatal hepatotoxic condition. We have studied the protective effect of chitosan supplementation against the hepatotoxicity induced by antitubercular drugs with respect to the changes in the levels of protein, albumin-globulin ratio, urea and bilirubin in the serum and diagnostic marker enzymes (alanine amino transferase, aspartate amino transferase, acid phosphatase and alkaline phosphatase), protein, glycoprotein conjugates (hexose, hexosamine and sialic acid), lipid peroxidation and reduced glutathione in the liver tissue of normal and experimental groups of rats. Co-administration of chitosan was found to significantly prevent the antitubercular drugs-induced alterations in the levels of diagnostic marker enzymes, bilirubin and albumin/globulin ratio in experimental groups of rats. Isoniazid and rifampicin-induced lipid peroxidation was also found to be prevented by the administration of chitosan. Further, chitosan administration increased the levels of urea and protein (in serum and liver) in experimental groups compared to hepatotoxicity-induced group of rats. Levels of glycoconjugates were also maintained to near normal level by chitosan co-administration. From the results obtained, it can be concluded that chitosan is beneficial against antitubercualr drugs-induced hepatoxicity.

The present study examined the changes occurring in the pro phenoloxidase system and antioxidant defence status in haemolymph, hepatopancreas and muscle tissue of white spot syndrome virus (WSSV) infected Penaeus monodon. Tiger shrimps (P. monodon) were infected with white spot virus by intramuscular injection of the virus inoculum. Levels of lipid peroxides and the activities of phenoloxidase, glutathione-dependent antioxidant enzymes [glutathione peroxidase (GPX), glutathione-S-transferase (GST)] and antiperoxidative enzymes [superoxide dismutase (SOD) and catalase (CAT)] were determined. WSSV infection induced a significant increase in lipid peroxidation in haemolymph, muscle and hepatopancreas of experimental P. monodon compared to normal controls. This was paralleled by significant reduction in the activities of phenol oxidase, glutathione-dependent antioxidant enzymes and antiperoxidative enzymes. The results of the present study indicate that the tissue antioxidant defence system in WSSV infected P. monodon is operating at a lower rate, which ultimately resulted in the failure of counteraction of free radicals, leading to oxidative stress as evidenced by the increased level of lipid peroxidation.

The anti-ulcerogenic effect of chitin and chitosan against ulcer induced by HCl-ethanol in male Wistar rats was studied. Levels of acid output, pepsin, protein, lipid peroxides and reduced glutathione and the activity of glutathione peroxidase (GPx), glutathione-S-transferase (GST), catalase (CAT) and superoxide dismutase (SOD) were determined in the gastric mucosa of normal and experimental groups of rats. A significant increase in volume and acidity of the gastric juice was observed in the ulcer-induced group of rats. Peptic activity was significantly decreased as compared with that of normal controls. In the rats pre-treated with chitin and chitosan 2% along with feed, the volume and acid output and peptic activity of gastric mucosa were maintained at near normal levels. The level of lipid peroxidation was significantly higher in the ulcerated mucosa when compared with that of normal controls. This was paralleled by a decline in the level of reduced glutathione and in the activity of antioxidant enzymes like GPx, GST, CAT and SOD in the gastric mucosa of ulcer-induced rats. Also, the levels of mucosal proteins and glycoprotein components were significantly depleted in ulcerated mucosa. The pre-treatment with chitin and chitosan was found to exert a significant anti-ulcer effect by preventing all the HCl-ethanol-induced ulcerogenic effects in experimental rats.

The cardioprotective effect of the ethanol extract of Picrorrhiza kurroa rhizomes and roots (PK) on isoproterenol-induced myocardial infarction in rats with respect to lipid metabolism in serum and heart tissue has been investigated. Oral pre-treatment with PK (80 mg kg −1 day −1 for 15 days) significantly prevented the isoproterenol-induced myocardial infarction and maintained the rats at near normal status.

Oysters are highly esteemed sea food and considered a delicacy throughout the world. Yet this resource is not optimally utilised in several parts of the world. The aim of this study is to highlight its nutritional importance. Biochemical composition and nutritional attributes of oyster meat are discussed. Proximate composition, fatty acid and amino acid profiles and mineral content were determined in oysters (C rassostrea madrasensis ). Moisture, protein, fat, carbohydrate and ash contents in the oyster were 82.64%, 9.41%, 3.25% 3.2% and 1.01%, respectively and it was rich in macro-minerals and trace elements especially selenium. Polyunsaturated fatty acids (PUFA) were highest of the total lipids among which eicosapentaenoic acid, docosahexaenoic acid and linoleic acid were the prominent fatty acids. The n -3/ n -6 index was high indicating a predominance of n -3 fatty acids in the species. Total amino acid content was 99.33 g/100 g crude protein, of which, essential amino acid lysine was the most abundant. Valine had the lowest essential amino acid score (EAAS) (0.17) while threonine had the highest EAAS of 3.62. Chemical score was 17% and the lowest limiting amino acid was valine. Protein efficiency ratio, essential amino acid index and biological value of oyster were 3.92, 120.2 and 174.0, respectively which indicates that the protein is of superior quality. Data on biochemical composition, nutritional attributes and quality indices of C. madrasensis protein may prove important for future policies regarding exploitation of this species and for inducing favourable changes in consumer preferences.

The hepatoprotective effect of the ethanol extract of Picrorrhiza kurroa rhizomes and roots (PK) on liver mitochondrial antioxidant defense system in isoniazid and rifampicin-induced hepatitis in rats was investigated. In liver mitochondria of antitubercular drugs administered rats, a significant elevation in the level of lipid peroxidation with concomitant decline in the level of reduced glutathione and in the activities of antioxidant enzymes was observed. Co-administration of PK (50 mg/kg/day for 45 days)significantly prevented these antitubercular drugs-induced alterations and maintained the rats at near normal status.