Daya Shankar Lal Srivastava

Pandit Bhagwat Dayal Sharma Post Graduate Institute of Medical Sciences

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Rama Devi Mittal

Sanjay Gandhi Post Graduate Institute of Medical Sciences

Anil Mandhani

Fortis Memorial Research Institute

Guy Brock

The Ohio State University

Oyeyemi Komolafe

Western Infirmary

Dhruva K. Mishra

Charles R. Drew University of Medicine and Science

La Creis R. Kidd

University of Louisville

Tiva Templeton

Baxter (United States)

Brandon Thacker

University of Louisville

David W. Hein

University of Louisville

P. Anandhi

Tamil Nadu Agricultural University

Cooperative Institutions

University of Louisville

Central Drug Research Institute

Istanbul University

Johns Hopkins University

Başkent University

Baxter (United States)

Council of Scientific and Industrial Research

National Cancer Institute

Institute of Medical Sciences

University of Michigan–Ann Arbor

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Population dynamics and evaluation of certain bio-products against brinjal leafhopper, Amrasca bigutulla bigutulla in Allahabad condition

Journal of Entomological Research (2011)

Savita Varma P. Anandhi Daya Shankar Lal Srivastava Yajuvendra Singh

The incidence of leafhopper Amrasca bigutulla bigutulla on brinjal commenced from 6th week after sowing i.e. second week of October (41st standard week) with an average population level of 0.03 leafhopper/plant during 1st year and in 2nd year it started from second week of October (41st standard week) with an average population level of 0.15 leafhopper/leaf. Maximum population of leafhopper was observed during February (5th week) to March (1st week). The leafhopper incidence showed positive correlation with maximum relative humidity, rainfall, wind speed and sunshine hrs. Chlorpyriphos was significantly superior as compared to botanicals.

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Free radical injury and antioxidant status in patients with benign prostate hyperplasia and prostate cancer

Indian Journal of Clinical Biochemistry (2005)

Daya Shankar Lal Srivastava Rama Devi Mittal

Malondialdehyde

10.1007/bf02867419

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Variant Base Excision Repair Genes (hOGG1, APE1, XRCC1) and Prostate Cancer Risk in African‐American Men

The FASEB Journal (2007)

Daya Shankar Lal Srivastava Oyeyemi Komolafe Tiva Templeton J. Christopher States Guy Brock

DNA damage induced by reactive oxygen species may be repaired by a complex network of base excision repair (BER) enzymes. BER enzymes (hOGG1, APE1 and XRCC1) are involved in sequential reactions that recognize and repair the damage resulting from oxidative stress. This study evaluated the individual and joint modifying effects of three highly variant BER genes in relation to prostate cancer risk within a large and unique prostate cancer case-control study of 918 African-American (AA) men. We hypothesize individuals who possess at least one variant hOGG1 326Cys allele in combination with one or more variant BER alleles (APE1 148Glu, XRCC1 399Glu) will have an increased prostate cancer risk, presumably due to reduced DNA repair capacity. Genetic alterations detected in germ-line DNA collected from 220 incident PCA cases and 698 healthy age matched controls were assessed using TaqMan real-time polymerase chain reaction. The intricate gene-gene interaction was analyzed using logistic regression analysis models, adjusted for age and PSA levels. We did not observe a significant role for individual BER high-risk alleles alone (P ≥ 0.215) or combined (P ≥ 0.509) in relation to prostate cancer risk among AA men. To expand our current efforts, future studies will consider the complex genetic architecture of prostate cancer, involving additional BER genes (e.g., XRCC3, XRCC4, MBD4, UNG). Bales Medical Research Fund

XRCC1

XRCC3

10.1096/fasebj.21.5.a421-d

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Polymorphism of glutathione S-transferase M1 and T1 genes and susceptibility to psoriasis disease: A study from North India

Indian Journal of Dermatology Venereology and Leprology (2017)

Daya Shankar Lal Srivastava Vijay Kumar Jain Poonam Verma Jaya Parkash Yadav

Increased oxidative stress and resulting inflammation has been emphasized as a factor in the pathogenesis of many diseases including psoriasis. Glutathione S-transferases (GSTs) protect against oxidative stress, inflammation, and genotoxicity. Polymorphisms in the GST genes may lead to an imbalance in pro- and antioxidant systems resulting in the increased production of reactive oxygen species that could influence the pathogenesis of psoriasis.The aim of this study was to investigate the association between GSTs (GSTM1 and GSTT1) gene polymorphism in patients with chronic plaque psoriasis as a factor in the susceptibility and development of psoriasis.We assessed 128 patients with psoriasis and 250 age- and sex-matched healthy controls. Genomic DNA was extracted from peripheral blood by the phenol chloroform method. The null GSTT1 and GSTM1 genotypes were identified by multiplex polymerase chain reaction (PCR) method.The null genotype of GSTM1 and GSTT1 was seen in 45.3% and 40.6% in psoriasis patients whereas in the controls it was 34.4% and 20.0%, respectively. A significant association was seen between the null alleles of the GSTT1 (OR = 2.74) and GSTM1 (OR = 1.58) alone or in combination with tobacco use (P < 0.001) and psoriasis risk. The presence of both null genotypes of GSTM1 and GSTT1 further increased the risk of psoriasis (OR = 3.52) when compared with the positive genotypes of GSTM1 and GSTT1.A major limitation of this study was the small sample size. A large epidemiological study is necessary to confirm these findings.The null genotype of GSTT1 is a strong predisposing factor for psoriasis in North India.

Pathogenesis

Glutathione S-transferase

Gene polymorphism

10.4103/ijdvl.ijdvl_1128_16

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Genetic polymorphism of drug metabolizing enzymes (CYP2E1, GSTP1) and susceptibility to bladder cancer in North India.

PubMed (2005)

Rama Devi Mittal Daya Shankar Lal Srivastava Anil Mandhani Bharat B. Mittal

Glutathione-S-transferases (GSTs) are active in the detoxification of wide variety of endogenous or exogenous carcinogens and genetic polymorphisms of CYP2E1 and GSTP1 genes have been studied extensively to evaluate the relative risk of various cancers. In the present study, we examined associations with CYP2E1 and GSTP1 gene polymorphisms in sporadic bladder cancers from North Indian patients. The subjects were 106 bladder cancer (Ca-B) cases and 162 age-matched controls. The GSTP1 313 A/G polymorphism was determined by the PCR/RFLP method using peripheral blood DNA. Binary Logistic Regression Model was used for assessing differences in genotype prevalence and their associations between patient and the control group. We observed a non-significant association in Pst1 polymorphism of the CYP2E1 gene; though the A/G genotype (OR = 2.69, 95% CI=1.57- 4.59, P= 0.000) and G/G genotype (OR = 7.68, 95% CI=2.77- 21.26, P= 0.000) of the GSTP1 gene polymorphism alone or in combination with tobacco users were highly significant (OR=24.06; 95% CI: 4.80- 120.42; P =0.000) when compared to the controls. The results of our study demonstrated that the GSTP1 313 G/G polymorphism is a strong predisposing risk factor for bladder cancer in the North Indian population.

GSTP1

Glutathione S-transferase

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Genetic polymorphism of glutathione S‐transferase genes (GSTM1, GSTT1 and GSTP1) and susceptibility to prostate cancer in Northern India

BJU International (2004)

Daya Shankar Lal Srivastava Anil Mandhani Balraj Mittal Rama Devi Mittal

OBJECTIVE To examine the association of glutathione‐S‐transferase (GST) gene polymorphisms in patients with sporadic prostate cancer, in a North Indian population, as GSTs are active in detoxifying a wide variety of endogenous or exogenous carcinogens, and genetic polymorphisms of GSTM1, GSTT1 and GSTP1 have been assessed to evaluate the relative risk of various cancers. PATIENTS AND METHODS We assessed 127 patients with prostate cancer and 144 age‐matched controls, all from North India. The GSTT1 and GSTM1 null genotypes were identified by multiplex polymerase chain reaction (PCR) in peripheral blood DNA samples, and GSTP1‐313 A/G polymorphism was determined by PCR/restriction fragment length polymorphism. RESULTS There was a significant association in null alleles of the GSTM1 (odds ratio 2.239, 95% confidence interval 1.37–3.65, P = 0.001) and GSTT1 (1.891, 1.089–3.282, P = 0.026) with prostate cancer risk, and in the ‐313 G alleles (Val) of the GSTP1 gene (2.48, 1.51–4.08, P < 0.001). The combined analysis of these three genotypes showed a further increase in the risks of prostate cancer (7.23, 2.42–22.6, P < 0.001). CONCLUSION The GSTP1‐313 G polymorphism, and null alleles of GSTM1 and GSTT1, are strong predisposing risk factors for sporadic prostate cancer in North India.

GSTP1

Glutathione S-transferase

10.1111/j.1464-410x.2005.05271.x

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Challenges Faced by Farmer Producer Organizations and Suggested Policy Reforms

Journal of Community Mobilization and Sustainable Development (2023)

Shailendra Kumar Singh Reema Devi Sachin Pratap Tomar Daya Shankar Lal Srivastava Anand Kumar Singh

10.5958/2231-6736.2023.00024.8

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GSTM1/GSTT1 Gene Polymorphism in North Indian Population and their Association to Hypertension

Biosciences Biotechnology Research Asia (2017)

Ritambhara Ritambhara Anup Kumar Daya Shankar Lal Srivastava Sivakumar Vijayaraghavalu Munish Kumar

ABSTRACT: Hypertension has multifactorial background and is a life style related disorder. Arterial hypertension is one of the most common types of hypertension and associated to oxidative stress known to be implicated in its pathogenesis. Glutathione S-transferases (GSTs) are phase II detoxification enzymes that play an important role in cellular defense against oxidative. GSTT1 and GSTM1 gene polymorphisms are reported to be associated with arterial hypertension in several populations and ethnic groups. GSTM1and GSTT1null genotype results in the impaired enzyme activity and consequently greater vulnerability towards various diseases such as cancer. The present study has been done to assess whether GSTT1 and GSTM1 null genotypes are associated with arterial hypertension among North Indian population. We have enrolled 99 arterial hypertension patients and 99 age and sex matched control individuals. Genotyping of GSTM1 and GSTT1 was done by multiplex PCR. We found that GSTM1 null genotype may have risk for hypertension (OR 1.75, CI 0.93-3.2), while for GSTT1 null genotypes shows protection toward hypertension (OR 0.254, CI-0.113-0.57). GSTM1 null genotypes serve as potential genetic factor and may be an independent risk factor for development of hypertension whereas GSTT1 null may have role in protection against hypertension in North Indian populations.

10.13005/bbra/2569

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Synthesis and antihyperglycemic activity of phenolic C-glycosides

Bioorganic & Medicinal Chemistry Letters (2010)

Preeti Rawat Manmeet Kumar Neha Rahuja Daya Shankar Lal Srivastava Arvind K. Srivastava

Blood sugar

10.1016/j.bmcl.2010.11.031

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Interaction among Carcinogen‐biotransformation Genes (N‐acetyltransferase 1 and 2) and Prostate Cancer Risk Using a Comprehensive Analytical Approach

The FASEB Journal (2007)

Tiva Templeton Brandon Thacker Daya Shankar Lal Srivastava Oyeyemi Komolafe Vasyl Pihur

Prostate cancer (PCA) incidence and mortality are highest among African-American (AA) men. Its detection and disparities could be improved through the identification of genetic susceptibilities within essential biological pathways. Interactions among highly variant N-acetyltransferase (NAT) genes, central to carcinogen-biotransformation pathways, modulate susceptibility to environmentally induced cancers, as demonstrated in previous reports. This study evaluates the interplay between two highly variant biotransformation genes (i.e., NAT1 and NAT2) and their influence on prostate cancer risk within a large and unique PCA case-control study of 918 AA men. The intricate interaction between polymorphic NAT1 and NAT2 was analyzed using conventional logistic regression analysis (LR) complemented with multiple dimensionality reduction. We hypothesize individuals who inherit two or more high-risk NAT alleles (e.g., NAT1*10 and slow NAT2*5) will have an increased risk of developing prostate cancer. Despite the relatively high prevalence (68.6–87.1%) of the high-risk NAT1*10 and slow NAT2 alleles among our study participants, their interaction did not significantly modify prostate cancer risk (P = 0.099). Future studies will evaluate the complex interplay among variant biotransformation and DNA repair genes and their joint modifying effects on prostate cancer risk. NCI 3RO1 CA034627-19S

Multifactor dimensionality reduction

N-acetyltransferase

10.1096/fasebj.21.5.a416-a

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