Subhash Chandra Mukherjee

Bio: Subhash Chandra Mukherjee is an academic researcher from Medical College and Hospital, Kolkata. The author has contributed to research in topics: Arsenic contamination of groundwater & Population. The author has an hindex of 21, co-authored 28 publications receiving 2798 citations. Previous affiliations of Subhash Chandra Mukherjee include Jadavpur University.

Arsenic Groundwater Contamination in Middle Ganga Plain, Bihar, India: A Future Danger?

Abstract: The pandemic of arsenic poisoning due to contaminated groundwater in West Bengal, India, and all of Bangladesh has been thought to be limited to the Ganges Delta (the Lower Ganga Plain), despite early survey reports of arsenic contamination in groundwater in the Union Territory of Chandigarh and its surroundings in the northwestern Upper Ganga Plain and recent findings in the Terai area of Nepal. Anecdotal reports of arsenical skin lesions in villagers led us to evaluate arsenic exposure and sequelae in the Semria Ojha Patti village in the Middle Ganga Plain, Bihar, where tube wells replaced dug wells about 20 years ago. Analyses of the arsenic content of 206 tube wells (95% of the total) showed that 56.8% exceeded arsenic concentrations of 50 micro g/L, with 19.9% > 300 micro g/L, the concentration predicting overt arsenical skin lesions. On medical examination of a self-selected sample of 550 (390 adults and 160 children), 13% of the adults and 6.3% of the children had typical skin lesions, an unusually high involvement for children, except in extreme exposures combined with malnutrition. The urine, hair, and nail concentrations of arsenic correlated significantly (r = 0.72-0.77) with drinking water arsenic concentrations up to 1,654 micro g/L. On neurologic examination, arsenic-typical neuropathy was diagnosed in 63% of the adults, a prevalence previously seen only in severe, subacute exposures. We also observed an apparent increase in fetal loss and premature delivery in the women with the highest concentrations of arsenic in their drinking water. The possibility of contaminated groundwater at other sites in the Middle and Upper Ganga Plain merits investigation.

Chronic Arsenic Toxicity in Bangladesh and West Bengal, India—A Review and Commentary

Abstract: Fifty districts of Bangladesh and 9 districts in West Bengal, India have arsenic levels in groundwater above the World Health Organization's maximum permissible limit of 50 μg/L. The area and popul...

Groundwater arsenic contamination and its health effects in the Ganga-Meghna-Brahmaputra plain.

Abstract: School of Environmental Studies, Jadavpur University, Kolkata, India Department of Neurology, Medical College, Kolkata, India Department of Obstetrics and Gynaecology, Institute of Post Graduate Medical Education and Research, S.S.K.M. Hospital, Kolkata, India Retired Professor of Dermatology, School of Tropical Medicine, Kolkata Department of Dermatology, Institute of Post Graduate Medical Education and Research, S.S.K.M. Hospital, Kolkata, India Dhaka Community Hospital, Dhaka, Bangladesh

Neuropathy in Arsenic Toxicity from Groundwater Arsenic Contamination in West Bengal, India

Abstract: Large number of people from 9 out of 18 districts of West Bengal, India are endemically exposed to arsenic contaminated groundwater due to drinking of tubewell water containing arsenic level above World Health Organization's maximum permissible limit of 50 microg/L. From our ongoing studies on neurological involvement in patients of arsenicosis from different districts of West Bengal, we report our findings in a total of 451 patients of three districts (Murshidabad, Nadia, and Burdwan), comprising 267 males and 184 females with age ranging from 11 to 79 years. They all had arsenical skin lesions, positive biomarkers and identified source of arsenic contaminated water drinking. Peripheral neuropathy was the predominant neurological complication in these patients affecting 154 (37.3%) of 413 patients of Group 1 and 33 (86.8%) of 38 patients of Group 2. Other possible causes and alternative explanations of neuropathy were excluded. The temporal profile in most of the cases (154 of Group 1) were of chronic affection while the 33 patients of Group 2 developed both neuropathy and dermopathy subacutely. Subacutely affected Group 2 patients had much higher incidence of neuropathy. Paresthesias and pains in the distal parts of extremities were much higher in incidence in Group 2 (73.7% and 23.7% respectively) than in Group 1 (18.4% and 11.1%). Distal limb weakness or atrophy was evident in 7.3% in Group 1 and 10.5% in Group 2. Overall, sensory features were more common than motor features in patients of neuropathy and sensory neuropathy was diagnosed in 30% and 76.3% and sensorimotor in 7.3% and 10.5% respectively in Group 1 and Group 2 subjects. Nerve conduction and electromyographic studies performed in 88 cases revealed dysfunction of sensory nerve in 45% and 27% and of motor nerve in 20% and 16.7% of patients with moderate degree and mild degree of clinical neuropathies respectively. Evoked potential studies performed in 20 patients were largely normal except for two instances each of abnormal visual evoked potential and brainstem auditory evoked potential findings. Prognosis was favorable in mild and early diagnosed cases of neuropathy whereas most of the other more severe and late diagnosed cases showed slow and partial recovery or even deterioration. Outcome in neuropathic patients of arsenicosis and long term toxic neurologic effects yet unexplored and unknown remain as matters of future concern requiring close monitoring.

Lipid peroxidation: production, metabolism, and signaling mechanisms of malondialdehyde and 4-hydroxy-2-nonenal.

Abstract: Lipid peroxidation can be described generally as a process under which oxidants such as free radicals attack lipids containing carbon-carbon double bond(s), especially polyunsaturated fatty acids (PUFAs). Over the last four decades, an extensive body of literature regarding lipid peroxidation has shown its important role in cell biology and human health. Since the early 1970s, the total published research articles on the topic of lipid peroxidation was 98 (1970–1974) and has been increasing at almost 135-fold, by up to 13165 in last 4 years (2010–2013). New discoveries about the involvement in cellular physiology and pathology, as well as the control of lipid peroxidation, continue to emerge every day. Given the enormity of this field, this review focuses on biochemical concepts of lipid peroxidation, production, metabolism, and signaling mechanisms of two main omega-6 fatty acids lipid peroxidation products: malondialdehyde (MDA) and, in particular, 4-hydroxy-2-nonenal (4-HNE), summarizing not only its physiological and protective function as signaling molecule stimulating gene expression and cell survival, but also its cytotoxic role inhibiting gene expression and promoting cell death. Finally, overviews of in vivo mammalian model systems used to study the lipid peroxidation process, and common pathological processes linked to MDA and 4-HNE are shown.

Role of metal-reducing bacteria in arsenic release from Bengal delta sediments

Abstract: The contamination of ground waters, abstracted for drinking and irrigation, by sediment-derived arsenic threatens the health of tens of millions of people worldwide, most notably in Bangladesh and West Bengal1,2,3. Despite the calamitous effects on human health arising from the extensive use of arsenic-enriched ground waters in these regions, the mechanisms of arsenic release from sediments remain poorly characterized and are topics of intense international debate4,5,6,7,8. We use a microscosm-based approach to investigate these mechanisms: techniques of microbiology and molecular ecology are used in combination with aqueous and solid phase speciation analysis of arsenic. Here we show that anaerobic metal-reducing bacteria can play a key role in the mobilization of arsenic in sediments collected from a contaminated aquifer in West Bengal. We also show that, for the sediments in this study, arsenic release took place after Fe(iii) reduction, rather than occurring simultaneously. Identification of the critical factors controlling the biogeochemical cycling of arsenic is one important contribution to fully informing the development of effective strategies to manage these and other similar arsenic-rich ground waters worldwide.

Arsenic: toxicity, oxidative stress and human disease.

Abstract: Arsenic (As) is a toxic metalloid element that is present in air, water and soil. Inorganic arsenic tends to be more toxic than organic arsenic. Examples of methylated organic arsenicals include monomethylarsonic acid [MMA(V)] and dimethylarsinic acid [DMA(V)]. Reactive oxygen species (ROS)-mediated oxidative damage is a common denominator in arsenic pathogenesis. In addition, arsenic induces morphological changes in the integrity of mitochondria. Cascade mechanisms of free radical formation derived from the superoxide radical, combined with glutathione-depleting agents, increase the sensitivity of cells to arsenic toxicity. When both humans and animals are exposed to arsenic, they experience an increased formation of ROS/RNS, including peroxyl radicals (ROO•), the superoxide radical, singlet oxygen, hydroxyl radical (OH•) via the Fenton reaction, hydrogen peroxide, the dimethylarsenic radical, the dimethylarsenic peroxyl radical and/or oxidant-induced DNA damage. Arsenic induces the formation of oxidized lipids which in turn generate several bioactive molecules (ROS, peroxides and isoprostanes), of which aldehydes [malondialdehyde (MDA) and 4-hydroxy-nonenal (HNE)] are the major end products. This review discusses aspects of chronic and acute exposures of arsenic in the etiology of cancer, cardiovascular disease (hypertension and atherosclerosis), neurological disorders, gastrointestinal disturbances, liver disease and renal disease, reproductive health effects, dermal changes and other health disorders. The role of antioxidant defence systems against arsenic toxicity is also discussed. Consideration is given to the role of vitamin C (ascorbic acid), vitamin E (α-tocopherol), curcumin, glutathione and antioxidant enzymes such as superoxide dismutase, catalase and glutathione peroxidase in their protective roles against arsenic-induced oxidative stress.