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Curcumin, the yellow pigment in turmeric, is present in the rhizomes of the plant Curcuma longa. Mercury (HgCl2) induces various toxic effects in different organs of the body. The present work was undertaken to evaluate the beneficial effect of curcumin following mercuric chloride induced oxidative stress in rat brain. The antioxidative indices assayed were superoxide dismutase, glutathione peroxidase, glutathione reductase, thiobarbituric acidreactive substances and total –SH groups. Metabolic parameters like total protein, cholesterol, succinate dehydrogenase, adenosine triphosphatase and mercury levels were also measured. Mercury exposure resulted in a significant increase in thiobarbituric acid-reactive substances and mercury levels. Contrarily a decrease in the activities of most of those enzymes, total –SH groups, protein and cholesterol levels were noted. Curcumin administration reduced TBARS and mercury levels, whereas it enhanced the other enzyme activities, total –SH groups, proteins and cholesterol levels comparable to controls. In summary, curcumin administration protects different parts of the brain against mercuric chloride induced neurotoxicity. Introduction Mercury is released into the environment through various natural geological processes, such as volatilization of rocks, dissolution, and volcanic eruption as well as due to some anthropogenic activities like combustion of fossil fuels, incineration of waste, mining and industrial discharge (Agrawal and Baheri, 2007). The cellular mechanisms by which mercury compounds exert their neurotoxic action were obtained from in vitro studies. Sorg et al. (1998) proposed that the mechanism of mercury toxicity could be via binding to thiol groups. Mercury compounds can inactivate a number of enzymes by blocking the functional sites binding to -SH groups, which are part of the catalytic or binding domains. Mercury treatment induced the dramatic increase in reactive oxygen species accumulating in rat brain cell cultures, leading to increased lipid peroxidation, protein degradation, and finally to cell death (Sorg et al., 1998). Rats and mice injected with inorganic mercury were detected with mercury granules in the different regions of the nervous system (Neustadt and Pieczenik, 2007). Mercury treatment exerted significant increase in ROS only in the cortical region and marked dose dependent increase (2500-5600-fold) in total Hg in the different brain regions (Goering et al., 2002). Morphological changes and Hg accumulation are different between cerebral hemisphere and cerebellar astrocytes after mercury treatment cultured from newborn rats (Adachi and Kunimoto, 2005). Pregnant female rats exposed to a very low dose of inorganic mercury from prenatal day 0 continued to postnatal day 20, the highest Hg content was present in the infant hippocampus and cerebellum, whereas its content in maternal brain regions like cerebrum, cerebellum, brain stem, hippocampus and thalamus (Feng et al., 2004). However, the role of herbal antioxidants on metal exerted neurotoxicity is attained less attention. Hence, this study was proposed to investigate the ameliorative effect of curcumin powder on regional brain toxicity induced by mercury in the rat. Rao et al. (2009) also studied effects of Hg in different regions of male rat brain affecting it in a dose dependent manner and role of melatonin on its toxicity. Materials and Methods Male Wistar strain Albino rats (Rattus norvegicus), weighing 200-250gms were procured from Cadila Pharma, under the Animal maintenance and Registration No.167/1999/CPCSEA from the ministry of Social Justice and empowerment, Govt. of India. The rats were fed on the standard commercial laboratory chow and distilled water ad libitum and were housed in the plastic cages with good ventilation. Light dark conditions as well as temperature was maintained (12h: 12h and 26±2oC respectively) throughout the seasons. Animals were assigned to 5 groups of 8 rats each. Group I served as control and animals were provided with distilled water. Group II animals received (low dose) HgCl2 (2mg/kg body weight) orally. Group III was administered with 4 mg/kg body weight (high dose) of mercuric chloride. Group IV received curcumin alone (80mg/kg body weight) and Group V received curcumin along with high dose of HgCl2. All the treatments were administered for 2 months and on the 61st day the animals were weighed and necropsy was performed. The brain was dissected carefully and weighed. Experiments were carried out on cerebral hemisphere and cerebellum. Antioxidant parameters The antioxidant enzyme activities like superoxide dismutase (SOD, EC:1.15.1.1), glutathione reductase (GR, EC:1.6.4.2), glutathione peroxidase (GPx, EC:1.11.1.9) were analysed by the spectrophotometric method of Kakkar et al. (1984), modified method of Pagila and Valentine (1967) and the method of Carlberg and Mannervik (1985) respectively. Thiobarbituric acid-reactive substances (TBARS) were determined by Ohkawa et al., (1979). Biochemical parameters The methods of total (-SH), succinate dehydrogenase (SDH, EC:1.3.99.1) and adenosine triphosphatase (ATPase, EC:3.6.1.3) was carried out by the methods of Sedlak and Lindsey (1968), Beatty et.al., (1966) and Quinn and White (1968) respectively. Total proteins and Cholesterol were determined by the methods of Lowry et al., (1951) and Zlatkis et. al., (1953) respectively. Mercury levels in the brain were estimated using mercury analyzer (MA 5840, Electronic Corporation of India Ltd., Hyderabad) using acid digestion method followed by cold vaporization of the sample. Data were statistically analyzed by Student’s t-test and ANOVA. Results Antioxidant system. In the present study antioxidant enzymes such as SOD, GPx, and GR were significantly (P

Healthy adult female rats (Rattus norvegicus) were administered sodium fluoride (NaF) at the dose of 10 mg/ kg body weight and triphala at 30 mg/kg body weight orally. Both doses were given individually and also in combination for 30 days to investigate the fluoride toxicity in blood and its reversal by triphala. NaF feeding also brought about a significant decline in hemoglobin level, mean corpuscular volume (MCV), mean corpuscular hemoglobin (MCH) and mean corpuscular hemoglobin concentration (MCHC) and red blood cell (RBC), which suggested occurrence of anemia and probable effect on haemopoetic system. Significant increase in erythrocyte sedimentation rate (ESR) indicates toxic effects in the body. Increase in white blood cells (WBC) count significantly suggests adverse effect of NaF treatment on the immune system of the rats. Co-administration of triphala to fluoride treated rats resulted in a partial effects in blood and body weight due to its probable protective role. Thus, triphala mitigated NaF induced toxicity marginally in a rat model. INTRODUCTION Fluorine is one of the most active elements, which belong to halogen group with a atomic number 9. The mass number of its isotopes are 18 and 19 but only the natural isotope 19F is stable.1 Fluoride (F-) in water sources is known to induce both useful and harmful influences on human body. Excessive amount of F can cause fluorosis.2 It is one of the most electronegative ions commonly used in the pharmaceutical and agrochemical industries.3 Fluoride intoxication causes different disorders in the body including hepatotoxicity, nephrotoxicity, neurotoxicity, and cardiotoxicity,3,4 associated with oxidative stress and altered anti-oxidant defense mechanisms. Previous studies from our laboratories and others have indicated that, consumption of antioxidant, such as Triphala, may mitigate the fluoride-induced oxidative stress in different tissues of rats.5 It also appears to be beneficial in its free-radical scavenging actions beyond its stimulatory effects on antioxidant enzyme system.6,7 The current study was undertaken to scrutinize mitigative role of Triphala on fluoride induced blood toxicity. METHODS AND MATERIALS Animals: Mature female Wistar rats (Rattus norvegicus) weighing between 250 and 350gm were procured from ZydusCadila Health Care, Ahmedabad under the Animal Maintenance and Registration No. 167/PO/C/99/CPCSEA from the Ministry of Social Justice and Empowerment, Government of India. The animals were housed under standard temperature (24±1oC) at a 12-hr dark/light cycle. They were fed standard rodent food (Pranav Agro Industries, Vadodara, India) and water ad libitum. Experimental design: After a 15-day adaptation period, the animals were divided into five different groups (Table 1) of 15 each and caged separately. Based on our earlier studies,1 the following doses were given for 30 days. Group I (control) rats were maintained on standard diet. Group II was treated with Triphala alone (30mg/kg bw) orally. Group III was administered a dose of sodium fluoride (10mg/kg bw) orally. Group IV was given 10 mg/kg bw dose of NaF along with Triphala 30mg/kg bw orally. After 30 days, the rats were fasted overnight and sacrificed under mild ether anesthesia. The weight of the body were recorded, and blood was colored by cardiac puncture and it was allowed to clot for 1 hour at room temperature and thereafter serum was separated by centrifugation and used for various serum parameters. Table 1. Experimental Protocol Group Treatment and daily dose (15 rats in each group) Duration

This study was conducted to investigate effects of sodium fluoride (NaF) on brain (cerebral hemisphere) of rat and its possible amelioration by melatonin. Adult male Wistar rats (Rattus novergicus) were administered sodium fluoride (NaF) at the doses of 5 and 10 mg/kg body weight and melatonin 10 mg/kg body weight for 60 days. Gravimetric and biochemical indices were done of brain an also studied. The increased lipid peroxidation (LPO) indicated an oxidative stress and the elevated fluoride levels in brain tissue could be the result of the inhibition of antioxidant enzymes (SOD, CAT) in the brain region of rats fed with fluoride. These changes were correlated with accumulation of fluoride in the region. However, these effects were ameliorated by co-supplementation of melatonin along with NaF in rats, because of its antioxidant cascade phenomenon. INTRODUCTION The presence of fluorine in ground water is mainly a natural phenomenon and influenced by local and regional conditions.1 Intake of high levels of fluoride is known to cause structural deformities, altered activities of enzymes, and metabolic lesions in the brain of experimental animals. Fluorosis exhibits neurological problems such as a tingling sensation in the fingers and toes, nervousness and depression. In the advanced stages of fluorosis, neurological manifestations such as paralysis of the limbs, vertigo, spasticity in the extremities, and impaired mental acuity, are observed in human beings.2 Sharma et al.3 reported that inhabitants of certain villages in Sanganer Tehsil, Jaipur, India were found to be suffering from various neurological disorders due to high levels of Fin the ground water; the main neurological manifestations observed were headache, insomnia, lethargy, depression, polyuria and polydipsia. Effects of NaF on the expression of intracellular Ca2+ fluxes, apoptosis and the antagonism of taurine in murine neuron were reported.4,5 Melatonin is a methoxyindole synthesized within the pineal gland. The hormone has strong antioxidant action neurodegenerative disorders.6 Therefore, to test this hypothesis, the present study was designed to investigate the role of melatonin administration in fluoride induced neurotoxicity in rats. MATERIALS AND METHODS Animals: Mature male Wistar rats (Rattus norvegicus) weighing between 200 and 300gm were procured from ZydusCadila Health Care, Ahmedabad under the Animal Maintenance and Registration No. 167/PO/c/99/CPCSEA from the Ministry of Social Justice and Empowerment, Government of India. The animals were housed under standard temperature (24±1oC) at a 12-hr dark/light cycle. They were fed standard rodent food (Pranav Agro Industries, Vadodara, India) and water ad libitum. Experimental protocol: After 15 days adaptation period, the animals were divided into five different groups (Table 1) of 15 each and caged separately. Based on our earlier studies,7 the following doses were given to rats for 60 days. After 60 days, the rats were fasted overnight and sacrificed under mild ether anesthesia. The weight of cerebral hemisphere was recorded, and the tissue was utilized for the estimation of different biochemical parameters. Table 1. Experimental Protocol Group Treatment and daily dose (15 rats in each group) Duration (days) Day of autopsy I Untreated (control) Sacrificed with treated