CURRY LEAVES AS ALTERNATIVE MEDICINE IN HEAVY METAL INDUCED OCCUPATIONAL HEALTH HAZARDS

Workers in different industries are regularly exposed to heavy metals. Those metals enter their body through several routes (inhalation, food contamination etc.,) and accumulate in the tissues and induce generation of reactive oxygen species (ROS) leading to oxidative damages. Chronic, regular exposures result in health hazards. Certain physiological, biochemical and behavioural dysfunctions cumulate to pathological conditions. Many of the symptoms complained by those industry workers are hardly recognized to be related to occupational exposure to heavy metals, often unidentified as occupational health hazards with a story of metal induced oxidative stress beneath their etiology. Most of the synthetic conventional drugs which are extensively prescribed by clinicians for treatments of these diseases have adverse side effects and potent cytotoxicity. Herbal remedy can be a safe substitute. The heavy metals induce generation of ROS and the phyto-components have the potential to scavenge those and boost the body's endogenous antioxidant system. They have no reported cytotoxic or adverse side effects, if not over consumed. Some specific or a perfect blend of potent phyto-constituent(s) from curry leaves can be suggested for or adapted as alternative medicine or integrative medicine for preventing or treating or curing or protecting against heavy metal-induced occupational health hazards

AQUEOUS BARK EXTRACT OF TERMINALIA ARJUNA PROTECTS AGAINST PHENYLHYDRAZINE INDUCED OXIDATIVE DAMAGE IN GOAT RED BLOOD CELL MEMBRANE BOUND AND METABOLIC ENZYMES

Objective: The objective of the present study is to determine the phenylhydrazine (PHZ) induced oxidative stress mediated alteration in the metabolic status and morphology of the red blood cells (RBC) and amelioration of the same by aqueous bark extract of Terminalia arjuna (TA).Methods: Fresh goat blood collected from local Kolkata Corporation approved slaughter house, was used for the present study. Packed cells were prepared from the freshly collected goat blood and were divided into four groups as follows for further studies i. e Group I: Control (CON), Group II: TA bark extract treated, named T5C (5 mg/ml, incubation mixture; positive control), Group III: PHZ treated (1 mM), Group IV: PHZ treated+TA bark extract at a dose of 5 mg/ml, named as P+T5. ROS, superoxide anion radical, and hydroxyl radical scavenging activity were determined. Intracellular iron and intracellular nitrate concentration were estimated. Activities of various membrane-bound enzymes like Na+/K+-ATPase, Mg2+-ATPase and Ca2+-ATPase and Ach-E were determined. Moreover, the activities of some metabolic enzymes like glucose 6-phosphate dehydrogenase (G6PDH), hexokinase, aldolase, lactase dehydrogenase were also studied. In addition, the morphological structure of RBCs was also determined.Results: PHZ treatment caused significant alterations in RBC morphology as well as altered the activities of membrane-bound as well as metabolic enzymes. All these changes following oxidative stress were found to be ameliorated when the RBCs were co-treated with PHZ and aqueous bark extract of TA. However, aqueous bark extract of TA alone did not exhibit any such changes in RBC.Conclusion: The aqueous bark extract of TA ameliorates PHZ-induced oxidative damages in goat RBC possibly by an antioxidant mechanism(s). The aqueous bark extract of TA may have future therapeutic relevance in oxidative stress-induced damages in RBCs.Keywords: Antioxidant enzymes, Aqueous bark extract, Oxidative stress, Phenylhydrazine, Red blood cells, Terminalia arjun

SILYMARIN PROTECTS AGAINST COPPER-ASCORBATE INDUCED INJURY TO GOAT CARDIAC MITOCHONDRIA IN VITRO: INVOLVEMENT OF ANTIOXIDANT MECHANISM(S)

Silymarin, 'one of the component of the Milk thistle seeds Silybum marianum (L.) is used in traditional food and medicine in India. In the present study, we investigated the antioxidant activities of Silymarin against copper-ascorbate induced toxic injury to mitochondria obtained from goat heart, in vitro. Incubation of isolated cardiac mitochondria with copper-ascorbate resulted in elevated levels of lipid peroxidation and protein carbonylation of the mitochondrial membrane, a reduced level of mitochondrial GSH and altered status of antioxidant enzymes as well as decreased activities of pyruvate dehydrogenase and the Kreb's cycle enzymes, altered mitochondrial morphology, mitochondrial swelling and di-tyrosine level. All these changes were found to be ameliorated when the cardiac mitochondria were co-incubated with copper-ascorbate and Silymarin, in vitro. Silymarin, in our in vitro experiments, was found to scavenge hydrogen peroxide, superoxide anion free radicals, hydroxyl radicals and DPPH radical, in a chemically defined system, indicating that this compound may provide protection to cardiac mitochondria against copper-ascorbate induced toxic injury through its antioxidant activities. The results of this study suggest that Silymarin may be considered as a future therapeutic antioxidant and may be used singly or as a co-therapeutic in the treatment of diseases associated with mitochondrial oxidative stress

Effect of isoproterenol on lipid peroxidation and antioxidant enzymes of myocardial tissue of mice and protection by quinidine

Administration of isoproterenol to mice at a dose of 30 mg/100 g body weight for 3 consecutive days at an interval of 24 h induced lipid peroxidation in cardiac tissue and exhibited a significantly elevated serum glutamate oxaloacetate transaminase (SGOT) level. Increased superoxide dismutase (SOD) activity with a concomitant decrease in catalase activity has also been observed in cardiac tissue with isoproterenol treatment. Quinidine, a class I antiarrhythmic agent has been found to exhibit a protective role in isoproterenol induced myocardial ischaemia. Cardiac tissue of quinidine treated mice showed reduction of lipid peroxidation reaction. In addition, quinidine treatment is found to influence the cardiac antioxidant enzymes – catalase and SOD. The decrease of SOD activity and increase of catalase activity suggests that quinidine also exerts an ‘indirect antioxidant’ effect in protecting the myocardial tissue from reactive oxygen species. Furthermore, our current in vitro studies with quinidine have clearly shown in this work that it possesses a very convincing hydroxyl radical scavenging potential with almost no ability to scavenge superoxide anion and hydrogen peroxide (H2O2) in vitro. Thus, our present investigation suggests that quinidine, when administered to mice, strengthens the antioxidant defense system to resist the free radical induced damage brought about by isoproterenol induced ischaemic condition. (Mol Cell Biochem 245: 43–49, 2003

Effect of Cu<SUP>2+</SUP>-ascorbic acid on lipid peroxidation, Mg<SUP>2+</SUP>-ATPase activity and spectrin of RBC membrane and reversal by erythropoietin

The effect of erythropoietin (Ep), a glycoprotein hormone, has been studied on lipid peroxidation induced by Cu2+ and ascorbate in vitro, Mg2+ ATPase activity and spectrin of RBC membrane. Our present investigation reveals that Cu2+ and ascorbic acid increases lipid peroxidation of RBC membrane significantly. It has further been observed that under the same experimental condition spectrin, a major cytoskeleton membrane protein, and Mg2+-ATPase activity of RBC membrane decrease significantly. However, exogenous administration of Ep completely restores lipid peroxidation and Mg2+-ATPase activity and partially recovers spectrin of RBC membrane

Melatonin protects against lead acetate induced oxidative stress-mediated changes in morphology and metabolic status in rat red blood cells: a flow cytometric and biochemical analysis

ABSTRACT Background: Lead is an abundantly occurring heavy metal known to be toxic in higher quantities for humans and other animals. Moreover, lead exposure has previously been shown to cause damage to red blood cell. However, a detailed study with a plausible mechanism is still lacking. The pineal hormone, melatonin, is well known for its antioxidant and free radical scavenging properties. Thus, we examined the effect of melatonin pre-treatment on lead acetate-induced toxicity in rat RBCs in vivo as well as in vitro and tried to find out the mechanism behind such protection. Main methods: Rats were injected intra-peritoneally with lead acetate (15mg/kg/day) for seven consecutive days in presence/ absence of melatonin (10mg/kg body weight). RBCs isolated from whole blood were haemolysed and was used for measuring changes in biochemical parameters and altered red blood cell morphology. Results &amp; Discussion: Rats injected intra-peritoneally with lead acetate (15mg/kg/day) for seven days exhibited an altered status of lipid peroxidation level, reduced glutathione content, protein carbonyl and oxidized glutathione levels along with inhibition of superoxide dismutase and catalase activities in RBCs indicating generation of oxidative stress. Data obtained using light microscopy, scanning electron microscopy and flow cytometry indicate deterioration of RBC morphology along with marked alterations in granularity. Atomic absorption spectrophotometric analysis revealed lead accumulation and reduction in iron and zinc levels along with decreased carbonic anhydrase and met haemoglobin reductase activities in RBCs isolated from lead acetate-treated rats. An increase in osmotic fragility and marked changes in the activities of the glutathione metabolising enzymes, hexokinase, glucose-6-phosphate dehydrogenase, aldolase, lactate dehydrogenase and acetylcholine esterase in RBC were also observed following lead acetate treatment. Rats pre-treated with melatonin (10mg/kg body weight) displayed restoration of these altered activities, suggesting its ameliorative action against lead acetate toxicity. Additionally, in vitro studies indicated that lead acetate-induced alterations of RBC enzyme activities are time and concentration-dependent and when co-incubated with melatonin, these changes were restored. Conclusion: The present study demonstrates the potential ability of melatonin to provide protection against lead acetate-induced injury to RBCs through its antioxidant properties in addition to removal of non-competitive inhibition of some of the enzymes