Agricure Biotech Research Society

Medinīpur, India

Agricure Biotech Research Society

Medinīpur, India
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Maiti S.,Oklahoma State University | Maiti S.,Agricure Biotech Research Society | Maiti S.,Vidyasagar University | Chen G.,Oklahoma State University
Archives of Physiology and Biochemistry | Year: 2015

Ethanol-consumption impairs physiological-efficiency/endurance, expedites senescence. Impaired-regulations of steroids/biomolecules link these processes. Steroids are catabolized by cytosolic-sulfotransferases (SULTs). Ethanol-induction of eukaryotic-SULTs-expression is scanty. Plant (Brassica-napus) steroid-sulfotransferase; BNST3/BNST4 (gene/BNST) is highly ethanol-inducible (protein/mRNA). Resembling mammalian-SULTs catalytic-mechanism BNSTs show broad substrate-specificities (mammalian-steroids; estradiol/dehydroepiandrosterone/pregnanolone). Recently, ethanol-regulation of SULTs-expression is verified in rat liver/intestine/cultured human-hepatocarcinoma (Hep-G2) cells at enzyme-activity/protein-expression (Western-blot) level. Here, two week's ethanol ingestion by male rat significantly increased SULT2A1 in their liver/intestine (p<0.05-p<0.001) and phenol-sulfotransferase (SULT1A1) in intestine (p<0.001) at enzyme-activity/protein levels. In human cells, ethanol significantly (2-fold) increased hSULT1A1/hSULT1E (2-3 fold) protein expressions paralleling their enzymatic-activities (p<0.05-p<0.01). The earlier finding of alcohol-association to the physiological impairment may be corroborated by our present findings. Inductions of SULT-expressions by ethanol have significant physiological/pharmacological consequences. © 2015 Informa UK Ltd. All rights reserved: reproduction in whole or part not permitted.

Sinha N.K.,Raja NL Khan Womens College | Chattopadhyay J.C.,Medical College and Hospital | Das P.K.,Medical College and Hospital | Maiti S.,Vidyasagar University | And 2 more authors.
Indian Journal of Community Health | Year: 2013

Background: Worldwide, anemia in pregnant women is associated with low birth-weight, perinatal and maternal mortality. The Childhood malnourishment results in ill-health and psychosocial problems. In the present study, prevalence of anemia is determined in a community-based cross-sectional survey (June 2010 to May 2011) in non-pregnant, psychologically fit and economically backward women (total 241, 15-49 years). Methods: The investigation is based on interviews on a pre-tested, semi-structured questionnaire after testing with Mental Status Examination. Body mass index is assessed to evaluate undernutrition and thinness. Data processing and descriptive statistics were done using the SPSS, 2010. The Pearson ÷2 and ANOVA tests were performed to predict the level of significance. Results: Anthropometric indices and hemoglobin level indicate that the prevalence of anemia (Hb<12 g/dl, WHO) is 69.7% (p<0.01), which is severe in malnourished individuals (30%). It is found that, the anemia status (primary and mild) is better correlated with undernutrition and thinness. It is also noticed that the moderate to severe anemia is more indicative to pathological state than physiological state in grade II/ III thinness. Likewise, anemia also occurring in normal or overweight group indicates, beside nutrition, influence of possible pathological, psychological or environmental factors are also occurring. Conclusion: Present findings necessitates extensive health program. An unplanned urbanization resulting unfriendly socio-demographic changes is more detrimental than natural adversity associated rudimentary character of a rural area. Beside supplementation, proper health awareness is more important at policy making level for global management of anemia.

Acharyya N.,Molecular Therapeutics | Chattopadhyay S.,Vidyasagar University | Maiti S.,Molecular Therapeutics | Maiti S.,Agricure Biotech Research Society
Journal of Environmental Science and Health - Part C Environmental Carcinogenesis and Ecotoxicology Reviews | Year: 2014

Green tea (Camellia sinensis; CS) strongly reverses/prevents arsenic-induced apoptotic hepatic degeneration/micronecrosis and mutagenic DNA damage in in vitro oxidant stress model and in rat as shown by comet assay and histoarchitecture (HE and PAS staining) results. Earlier, we demonstrated a link between carcinogenesis and impaired antioxidant system-associated mutagenic DNA damage in arsenic-exposed human. In this study, arsenic-induced (0.6 ppm/100 g body weight/day for 28 days) impairment of cytosolic superoxide-dismutase (SOD1), catalase, xanthine-oxidase, thiol, and urate activities/levels led to increase in tissue levels of damaging malondialdehyde, conjugated dienes, serum necrotic-marker lactate-dehydrogenase, and metabolic inflammatory-marker c-reactive protein suggesting dysregulation at the transcriptional/signal-transduction level. These are decisively restrained by CS-extract (≥10 mg/ml aqueous) with a restoration of DNA/tissue structure. The structural/functional impairment of dialyzed and centrifugally concentrated (6-8 kd cutoff) hepatic SOD1 via its important Cys modifications by H2O2/arsenite redox-stress and that protection by CS/2-mercaptoethanol are shown in in vitro/in situ studies paralleling the present Swiss-Model-generated rSOD1 structural data. Here, arsenite(3+) incubation (≥10-8 M + 10 mM H2O2, 2 hr) is shown for the first time with this low-concentration to initiate breakage in rat hepatic-DNA in vitro whereas, arsenite/H2O2/UV-radiation does not affect DNA separately. Arsenic initiates Fe and Cu ion-associated free-radical reaction cascade in vivo. Here, 10 M of Cu(2+)/Fe(3+)/As(3+) +H2O2-induced in vitro DNA fragmentation is prevented by CS (≥1 mg/ml), greater than the prevention of ascorbate or tocopherol or DMSO or their combination. Moreover, CS incubation for various time with differentially and already degraded DNA resulted from pre-incubation in 10 M As(3+)-H2O2 system markedly recovers broken DNA. Present results decisively suggest for the first time that CS and its mixed polyphenols have potent SOD1 protecting, diverse radical-scavenging and antimutagenic activities furthering to DNA protection/therapy in arsenic-induced tissue necrosis/apoptosis. © 2014 Copyright © Taylor & Francis Group, LLC.

Acharyya N.,Molecular Therapeutics | Acharyya N.,Vidyasagar University | Deb B.,Vidyasagar University | Chattopadhyay S.,Vidyasagar University | And 3 more authors.
Biological Trace Element Research | Year: 2015

Arsenic is a grade I human carcinogen. It acts by disrupting one-carbon (1C) metabolism and cellular methyl (−CH3) pool. The −CH3 group helps in arsenic disposition and detoxification of the biological systems. Vitamin B12 and folate, the key promoters of 1C metabolism were tested recently (daily 0.07 and 4.0 μg, respectively/100 g b.w. of rat for 28 days) to evaluate their combined efficacy in the protection from mutagenic DNA-breakage and tissue damages. The selected tissues like intestine (first-pass site), liver (major xenobiotic metabolizer) and lung (major arsenic accumulator) were collected from arsenic-ingested (0.6 ppm/same schedule) female rats. The hemo-toxicity and liver and kidney functions were monitored. Our earlier studies on arsenic-exposed humans can correlate carcinogenesis with DNA damage. Here, we demonstrate that the supplementation of physiological/therapeutic dose of vitamin B12 and folate protected the rodents significantly from arsenic-induced DNA damage (DNA fragmentation and comet assay) and hepatic and renal tissue degeneration (histo-architecture, HE staining). The level of arsenic-induced free-radical products (TBARS and conjugated diene) was significantly declined by the restored actions of several antioxidants viz. urate, thiol, catalase, xanthine oxidase, lactoperoxidase, and superoxide dismutase in the tissues of vitamin-supplemented group. The alkaline phosphatase, transaminases, urea and creatinine (hepatic and kidney toxicity marker), and lactate dehydrogenase (tissue degeneration marker) were significantly impaired in the arsenic-fed group. But a significant protection was evident in the vitamin-supplemented group. In conclusion, the combined action of folate and B12 results in the restitution in the 1C metabolic pathway and cellular methyl pool. The cumulative outcome from the enhanced arsenic methylation and antioxidative capacity was protective against arsenic induced mutagenic DNA breakages and tissue damages. © 2015, Springer Science+Business Media New York.

Das P.K.,Medical College Hospital | Maiti S.,Vidyasagar University | Maiti S.,Agricure Biotech Research Society | Sinha N.K.,Agricure Biotech Research Society | Sinha N.K.,Raja N L Khan Womens College
Neurology Psychiatry and Brain Research | Year: 2016

Human Immunodeficiency Virus (HIV) impairs the physiological, behavioral and social development of the infected-children. With the advent of better antiretroviral-therapies (ARTs), the infected children are surviving well beyond adolescence accompanying with complicated ramification of management with bio-psycho-social factors. Presently, 76 children (53 perinatally HIV+ and 23 of their HIV- sibling) are screened for psychiatric-morbidities with Developmental-Psychopathology-Check-List (DPCL) which is a modified version of widely used protocol 'Child Behavior Check List (CBCL)'. Positively screened for psychopathology was regarded as psychiatrically morbid. In South-East Asian perspective, this type of investigation is scanty. Here, we investigate and report the psychiatric-morbidity status of vertically HIV infected children with a longitudinal comparison to their HIV- sibling. The present results suggest that 42.1% of the study-population suffers from psychiatric morbidity. Among the HIV+, 45.28% suffer from psychiatric-morbid constituting emotional-disorder, 41.67%, conduct-disorder, 37.50%, somatization 33.33%, learning-disorder, 29.16%, whereas in the HIV- group, 34.79% suffers from psychiatric morbidity mainly with emotional disorder [87.50%]. The age as an independent variable is noticed to be associated significantly (p. <. 0.001) with psychiatric-morbidity. Other variables amongst sex, CD4+ count, living-status of parents, caregiver-status was found to have certain extent of association with psychiatric-status. The present comparison with the more reliable control like HIV- sibling will help for the first time, to characterize better the infection association of psychiatric-morbidity of the HIV+ children. Advances should be espoused for the better survival of HIV infected children with improved ARTs application incorporating with advanced psychiatric-services. © 2016 Elsevier GmbH.

Acharyya N.,Vidyasagar University | Sajed Ali S.,Vidyasagar University | Deb B.,Vidyasagar University | Chattopadhyay S.,Vidyasagar University | And 2 more authors.
Environmental Toxicology | Year: 2015

This study elucidates the protective role of Green tea (Camellia sinensis or CS) against arsenic-induced mutagenic DNA-breakage/intestinal (small) damages in female rats. Intestinal epithelial cells receive ingested arsenic initially. Though, the possibility of damages in this tissue is immense and the therapeutic strategies against this damage are of great concern, reports on either issue are scanty. Our earlier study on arsenic-exposed human unveils a link between carcinogenesis and mutagenic DNA damage. Here, we demonstrate that supplementation of CS-extract (10 mg/mL water) with NaAsO2 (0.6 ppm)/100 g b.w. for 28 days to rats offered a significant protection against arsenic-induced oxidative damages to DNA and intestinal (small) tissues by buttressing antioxidant systems. Necrotic and apoptotic damages and their CS-protection are shown in DNA-fragmentation, comet-assay, and histoarchitecture (hematoxylin and eosin and periodic acid-schiff staining) results. Only arsenic exposure significantly decreased intestinal superoxide dismutase, catalase activities, and level of soluble thiol with a concomitant increase in malondialdehyde/conjugated dienes. Alteration of serum necrotic marker lactate dehydrogenase and the metabolic inflammatory marker c-reactive protein also indicate the impairment may be occurring at transcription and/or cellular signal transduction level. In addition, in situ incubation in rat intestinal loop filled for 24 h with NaAsO2 alone (250 μM) or with aqueous CS-extract (250 mg/mL) suggests that small intestinal epithelial cells are significantly protected by CS against arsenic-associated necrotic/mutagenic damages, which is observed in DNA-breakage studies. In conclusion, besides intensifying endogenous antioxidant system, CS polyphenols also offer a direct role on free radical scavenging activity that is associated to the protection from mutagenic DNA-breakages and prevention of tissue necrosis/carcinogenesis generated by arsenic. © 2014 Wiley Periodicals, Inc.

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