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Lucknow, India

Industrial Toxicology Research Centre is now named as Indian Institute of Toxicology Research , Lucknow, India. The institute is engaged in the field of Toxicology having its main campus in Lucknow city and the other Gheru campus, is located near village 'Gheru' at Lucknow-Kanpur highway.It is one of the constituent laboratory of CSIR India, which was established in 1965 with the motto of "Safety to Environment & Health and Service to Industry". The founder Director of the institute was Prof. Sibte Hasan Zaidi who died on 5 April 2008 at New York. He was the recipient of Padmashri and prestigious Sir Shanti Swaroop Bhatnagar award for scientific excellence. IITR conducts Dr. S.H. Zaidi Oration in his honour every year during its foundation day celebrations on 4 November.The institute is dedicated towards research in Fundamental and Applied Toxicology. Major thrust areas include Environmental toxicology, Ground and surface water pollution, Safety assessment of food & additives, Toxicity evaluation of substances for human use, Microbial contaminations, Bioremediation, Hazard identification and Toxicogenomics.The institute attracts students from all over India to pursue research. IITR offers Ph.D. programme in various areas, few to name are In vivo & In vitro Toxicology, Environmental Toxicology, Genetic Toxicology, Immunotoxicology, Neurotoxicology, Food Toxicology, Environmental Microbiology and Carcinogenesis.The institute also offers services for Toxicological and Analytical evaluation of chemicals / finished products to public and private sectors as per OECD, USEPA, BIS, ISO guidelines.IITR, dream of a visionary, became a reality in 1965 as Industrial Toxicology Research Centre located in Central Drug Research Institute, Lucknow. The founder Director, Prof. Sibte Hasan Zaidi, could foresee the need to address health related to work environment of the industrial workers in post independence era of rapid industrialization in our country. It was advocated that the adverse effects of chemicals on health and environment will make an adverse impact on overall development of the country. Hence, studies were needed to develop strategies for sustainable industrial development. ITRC gained national importance by addressing the health problems of our industrial work force in a growing economy. Pioneering studies carried out during the formative years were directly linked to miners' health especially to respiratory ailments.Like a unique organism, the institute adapted and evolved to grow from strength to strength with addition of new activities and expertise. Today, research in Toxicology is at the crossroad of transformation from classical studies of animal experimentation and histological observations of animal tissues in late sixties to state of the art omic technologies in interdisciplinary area of biology. The concept of biomarkers, alternate to animal models, mathematical modelling and predictive toxicology are to name a few to make toxicological research intrinsic in protection of human health and environment. ITRC was rechristened as the Indian Institute of Toxicology Research in 2008 to empower research activities in new frontiers of toxicology considering the paradigm shifts in our understanding of human and environmental health. In the new millennium, the institute is poised to make an impact in understanding the mode of action of new chemical entities, engineered nanomaterials and genetically modified products on living systems for safe use of new technologies and sustainable development.IITR website endeavours to provide a reflection of our mission in the new millennium. Wikipedia.

A simple and rapid analytical method based on in-matrix ethyl chloroformate (ECF) derivatization has been developed for the quantitative determination of bisphenol-A (BPA) in milk and water samples. The samples containing BPA were derivatised with ECF in the presence of pyridine for 20 s at room temperature, and the non-polar derivative thus formed was extracted using polydimethylsiloxane solid-phase microextraction (SPME) fibres with thicknesses of 100 μm followed by analysis using gas chromatography-mass spectrometry. Three alkyl chloroformates (methyl, ethyl and isobutyl chloroformate) were tested for optimum derivatisation yields, and ECF has been found to be optimum for the derivatisation of BPA. Several parameters such as amount of ECF, pyridine and reaction time as well as SPME parameters were studied and optimised in the present work. The limit of detection for BPA in milk and water samples was found to be 0.1 and 0.01 μg L(-1), respectively, with a signal-to-noise ratio of 3:1. The limit of quantitation for BPA in milk and water was found to be 0.38 and 0.052 μg L(-1), respectively, with a signal-to-noise ratio of 10:1. In conclusion, the method developed was found to be rapid, reliable and cost-effective in comparison to silylation and highly suitable for the routine analysis of BPA by various food and environmental laboratories. Source

Singh M.,Indian Institute of Toxicology Research
Journal of biomedical nanotechnology | Year: 2011

Anti-cancer potential of polymer based nanoparticle of EGCG and TF alone and in combination with anti-cancer drug cisplatin have been studied in human cancer lines: A549 (lung carcinoma), HeLa (cervical carcinoma) and THP-1 (acute monocytic leukemia) using cell proliferation assay and cell cycle analysis. Encapsulated polyphenols retained biological effectiveness with over 20-fold dose advantage than EGCG/TF in exerting anti-cancer effects and also enhanced the potential of a widely used anti-cancer drug cisplatin. Subsequently, encapsulated polyphenols alone or in combination with cisplatin were more effective in inhibiting cell proliferation, metastasis, angiogenesis and apoptosis biomarkers. Collectively, our observations reveal that nanoparticle-mediated delivery of phytochemicals could serve as a basis for enhancing bioavailability and limiting the unwanted toxicity of chemotherapeutic agents. Source

Chaturvedi R.K.,Indian Institute of Toxicology Research | Beal M.F.,Cornell University
Molecular and Cellular Neuroscience | Year: 2013

Substantial evidence from both genetic and toxin induced animal and cellular models and postmortem human brain tissue indicates that mitochondrial dysfunction plays a central role in pathophysiology of the neurodegenerative disorders including Parkinson's disease (PD), and Huntington's disease (HD). This review discusses the emerging understanding of the role of mitochondrial dysfunction including bioenergetics defects, mitochondrial DNA mutations, familial nuclear DNA mutations, altered mitochondrial fusion/fission and morphology, mitochondrial transport/trafficking, altered transcription and increased interaction of pathogenic proteins with mitochondria in the pathogenesis of PD and HD. This review recapitulates some of the key therapeutic strategies applied to surmount mitochondrial dysfunction in these debilitating disorders. We discuss the therapeutic role of mitochondrial bioenergetic agents such as creatine, Coenzyme-Q10, mitochondrial targeted antioxidants and peptides, the SIRT1 activator resveratrol, and the pan-PPAR agonist bezafibrate in toxin and genetic cellular and animal models of PD and HD. We also summarize the phase II-III clinical trials conducted using some of these agents. Lastly, we discuss PGC-1α, TORC and Sirtuins as potential therapeutic targets for mitochondrial dysfunction in neurodegenerative disorders. This article is part of a Special Issue entitled 'Mitochondrial function and dysfunction in neurodegeneration'. © 2012 Elsevier Inc. Source

Shukla A.K.,Indian Institute of Toxicology Research
Neurobiology of aging | Year: 2014

Parkinson's disease (PD) is a prevalent and devastating neurodegenerative disorder having limited cure options and strong association with the loss of dopaminergic neurons in the substantia nigra region of the mid brain. Etiology of PD includes both genetic and environmental factors. Paraquat (PQ), a widely used herbicide, is known to be associated with pathogenesis of PD. We report that a mutation in Drosophila methuselah (mth(1)), which is associated with aging, has a role in preventing dopaminergic neuronal cell death in PQ-exposed organism. Exposed mth(1) flies exhibit significant resistance against PQ-induced Parkinson's phenotypes and behavior in terms of oxidative stress, dopaminergic neuronal degeneration, locomotor performance, dopamine content, phosphorylated JNK, pFOXO, Hid, and cleaved caspase-3 levels. Conversely, over-expression of mth in dopaminergic neurons makes the exposed organism more vulnerable to oxidative stress, neuronal cell death, and behavioral deficit. The study suggests that lesser activation of JNK-mediated apoptosis in dopaminergic neurons of exposed mth(1) flies protects the organism from PQ-induced damage, which may be causally linked to a common mechanism for PQ-induced neurodegeneration. Copyright © 2014 Elsevier Inc. All rights reserved. Source

Chaturvedi R.K.,Indian Institute of Toxicology Research | Chaturvedi R.K.,Academy of Scientific and Innovative Research AcSIR | Beal M.F.,Cornell University
Free Radical Biology and Medicine | Year: 2013

Neurodegenerative disorders are debilitating diseases of the brain, characterized by behavioral, motor and cognitive impairments. Ample evidence underpins mitochondrial dysfunction as a central causal factor in the pathogenesis of neurodegenerative disorders including Parkinson's disease, Huntington's disease, Alzheimer's disease, Amyotrophic lateral sclerosis, Friedreich's ataxia and Charcot-Marie-Tooth disease. In this review, we discuss the role of mitochondrial dysfunction such as bioenergetics defects, mitochondrial DNA mutations, gene mutations, altered mitochondrial dynamics (mitochondrial fusion/ fission, morphology, size, transport/trafficking, and movement), impaired transcription and the association of mutated proteins with mitochondria in these diseases. We highlight the therapeutic role of mitochondrial bioenergetic agents in toxin and in cellular and genetic animal models of neurodegen-erative disorders. We also discuss clinical trials of bioenergetics agents in neurodegenerative disorders. Lastly, we shed light on PGC-1α, TORC-1, AMP kinase, Nrf2-ARE, and Sirtuins as novel therapeutic targets for neurodegenerative disorders. © 2013 Elsevier Inc. All rights reserved. Source

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