13 research outputs found

    SPATIO-TEMPORAL VARIATION OF MERCURY IN BIDYADHARI RIVER OF SUNDARBAN DELTA, INDIA

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    Bidyadhari river originates in Nadia district of West Bengal, India and then flows through North 24 Parganas district and now serves as a sewage and excess rainwater outlet from the city of Kolkata and adjacent area, which ultimately empties at the Bay of Bengal through the Indian Sundarban delta. Four different stations situated around the course of the river at considerable distances have been selected from the outfall of sewage canals at Kulti-Ghushighata (S1), where metropolitan sewages discharged and mixed up into water of Bidyadhari river, which ultimately carried through this river via stations Malancha (S2), Kanmari (S3) to Dhamakhali (S4), just before the river confluences with the larger Raimangal river at northern Sundarban delta. This study was conducted to estimate total mercury (Hg) concentration in waters (during high tides and ebb tides) and sediments of Bidyadhari river in pre-monsoon, monsoon and post-monsoon seasons during the period from March, 2012 to February, 2013 at those stations. It is revealed from the estimated data that agricultural runoff, sewage, effluents from various industries and Kolkata metropolitan, Salt Lake City and adjacent areas of North 24 Parganas district carried and discharged in Bidyadhari river through sewage canals are not so high in mercury content for sediment contamination but alarming in respect of water quality, which crosses the permissible limit of Hg for consumption (0.001 ppm) in wide range of areas at Kanmari and Dhamakhali around the estuary. Enhancement of Hg level in this river water and transportation of the metal through tidal effects to and fro mangrove land of Sundarban may be dangerous for aquatic lives and supposed to be grave concern for the ecology of the Sundarban delta including human

    Experimental assessment of arsenic toxicity in garole sheep in India

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    Arsenic, a dangerous bio-accumulative poison, is a grave threat affecting a large number of people as well as animals throughout the World, particularly in Bangladesh and West Bengal, India. It is also a matter of concern as continuously entering into food chain through biotic and abiotic products. The present study was conducted to evaluate the experimental effect of arsenic toxicosis on Garole sheep of West Bengal. One group was subjected to oral arsenic exposure @ 6.6 mg Kg−1 over 133 days when rests considered as negative control. Periodical arsenic estimation in wool, urine and feces along with hemato-biochemical alteration were checked thoroughly. It was evident from the study that long term arsenic exposure exerted a significant (p < 0.01) alteration compared to normal animal which were further supported by clinical abnormalities. Exposed animals showed histological changes throughout major internal organs like coagulative necrosis of liver, tubular nephritis of kidney and acanthosis of skin etc. The bio-accumulative and excretion pattern of arsenic inside body were also well understood by the arsenic estimation study of wool, urine and feces which may be helpful for discussion regarding arsenic entry into food chain via animals

    Immunotoxic and genotoxic potential of arsenic and its chemical species in goats

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    The study investigated the immunotoxic and genotoxic effect of arsenic and its different species on goats. It was found that arsenic causes haematological crisis. Histopathological changes in spleen and reduced serum immunoglobulin G level without any changes in formazan production in arsenic-treated animals indicated that arsenic is toxic to the humoral immune system. Increased caspase-3 production and higher number of TUNEL (terminal deoxynucleotidyl transferase-mediated dUTP nick-end labelling)-positive bone marrow cells along with oligonucleosomal DNA fragmentation on agarose gel suggested apoptosis induction by arsenic in the bone marrow cells of goat. Total arsenic concentration in the plasma, bone marrow, and spleen of the exposed group was, respectively, 1.22 ± 0.11, 2.20 ± 0.21, and 3.39 ± 0.14 ppm. Speciation study revealed that arsenite and organoarsenic were the major arsenic species in these samples, suggesting their role in immunotoxic and genotoxic potential in goats

    Pro-Opiomelanocortin (POMC) neurons in the nucleus of the solitary tract mediate endorphinergic endogenous analgesia in mice

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    : The nucleus of the solitary tract (NTS) contains pro-opiomelanocortin (POMC) neurons which are one of the two major sources of β-endorphin in the brain. The functional role of these NTS POMC neurons in nociceptive and cardiorespiratory function is debated. We have shown that NTS POMC optogenetic activation produces bradycardia and transient apnoea in a working heart brainstem preparation and chemogenetic activation with an engineered ion channel (PSAM) produced opioidergic analgesia in vivo . To better define the role of the NTS POMC neurons in behaving animals, we adopted in vivo optogenetics (ChrimsonR) and excitatory/inhibitory chemogenetic DREADD (hM3Dq/hM4Di) strategies in POMC-Cre mice. We show that optogenetic activation of NTS POMC neurons produces time-locked, graded, transient bradycardia and bradypnoea in anaesthetised mice which is naloxone sensitive (1 mg/kg, i.p) suggesting a role of β-endorphin. Both optogenetic and chemogenetic activation of NTS POMC neurons produces sustained thermal analgesia in behaving mice which can be blocked by naloxone. It also produced analgesia in inflammatory pain (carrageenan) but not in a neuropathic pain model (tibial nerve transection). Inhibiting NTS POMC neurons does not produce any effect on basal nociception but inhibits stress-induced analgesia (unlike inhibition of arcuate POMC neurons). Activation of NTS POMC neuronal populations in conscious mice did not cause respiratory depression, anxiety or locomotor deficit (in open field) nor affective preference. These findings indicate that NTS POMC neurons play a key role in the generation of endorphinergic endogenous analgesia and can also regulate cardiorespiratory function

    Ameliorative effect of tephrosia purpurea in arsenic-induced nephrotoxicity in rats

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    OBJECTIVES: The present investigation was conducted to evaluate the nephroprotective activity of Tephrosia purpurea (TPE) against arsenic-induced toxicity. MATERIALS AND METHODS: Twenty four number of wistar rats were equally divided into three groups. Sodium arsenite (10 mg/kg) was orally given to group I for 28 days, additionally group II was orally treated with TPE (500 mg/kg), while the control group was kept untreated with neither arsenic nor TPE. Serum biomarker levels, oxidative stress indices and arsenic concentration in kidney were estimated. Histopathology of kidney was also conducted. RESULTS: Group II animals show significantly reduced blood urea nitrogen and plasma creatinine, and increased serum albumin level compared to group I. The higher lipid peroxidation with exhausted superoxide dismutase activity and reduced glutathione level were noticed in group I compared to group II. There was no significant difference in arsenic accumulation in kidneys between the two arsenic treated groups, but the histopathology of kidney of group II rats revealed reduced necrosis and intact tubular architecture as compared to group I. CONCLUSIONS: Tephrosia Purpurea extract has a significant role in protecting the animals from arsenic-induced nephrotoxicity

    Ameliorative Effect of Tephrosia Purpurea in Arsenic-induced Nephrotoxicity in Rats

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    OBJECTIVES: The present investigation was conducted to evaluate the nephroprotective activity of Tephrosia purpurea (TPE) against arsenic-induced toxicity. MATERIALS AND METHODS: Twenty four number of wistar rats were equally divided into three groups. Sodium arsenite (10 mg/kg) was orally given to group I for 28 days, additionally group II was orally treated with TPE (500 mg/kg), while the control group was kept untreated with neither arsenic nor TPE. Serum biomarker levels, oxidative stress indices and arsenic concentration in kidney were estimated. Histopathology of kidney was also conducted. RESULTS: Group II animals show significantly reduced blood urea nitrogen and plasma creatinine, and increased serum albumin level compared to group I. The higher lipid peroxidation with exhausted superoxide dismutase activity and reduced glutathione level were noticed in group I compared to group II. There was no significant difference in arsenic accumulation in kidneys between the two arsenic treated groups, but the histopathology of kidney of group II rats revealed reduced necrosis and intact tubular architecture as compared to group I. CONCLUSIONS: Tephrosia Purpurea extract has a significant role in protecting the animals from arsenic-induced nephrotoxicity

    Effect of Environmental Exposure of Arsenic on Cattle and Poultry in Nadia District, West Bengal, India

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    A study was undertaken to evaluate an alternative source of arsenicosis in human food chain through livestock. Thirty milch cattle and 20 poultry birds along with their eggs were selected randomly from two endemic villages of Nadia district and one nonendemic villages of Hooghly district in West Bengal, India. Milk, feces, urine, and hair samples of cattle and feed materials, such as water and straw, were collected to analyze arsenic status. Arsenic concentration in egg yolk and albumen from poultry eggs and different poultry organs after culling was estimated. Distribution of arsenic in animal body indicates that major portion of arsenic was eliminated through feces, urine, and milk. Poultry egg yolk, albumen, and poultry products retain arsenic in all organs. Cows and poultry birds reared in endemic zone retain significantly higher concentration of arsenic. Consumption of egg, agricultural produces grown in contaminated soil, and milk might have produced arsenicosis and may be considered as alternative source of arsenic contamination
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