GSTM1,GSTM3andGSTT1Gene Variants and Risk of Benign Prostate Hyperplasia in North India

Mittal, Rama Devi; Kesarwani, Pravin; Singh, Ranjana; Ahirwar, Dinesh K.; Mandhani, Anil

doi:10.1155/2009/568431

Cited by 11 publications

(8 citation statements)

References 27 publications

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“…Absence of these enzymes due to homozygous deletions is implicated in poor elimination of carcinogenic substances, making individuals with these deletions susceptible to oxidative injury [34] . A study has reported a positive association of GSTM1 or GSTT1 polymorphism with increased risk of BPH [35] . In individuals with BPH and with double deletions GSTM1 -/GSTT1 -, significantly higher MDA levels were observed compared to GSTM1 + / GSTT1 + [34] .…”

Section: Role Of Depletion Of Antioxidant Activitymentioning

confidence: 99%

Oxidative Stress in Benign Prostatic Hyperplasia: A Systematic Review

Minciullo

Inferrera²,

Navarra³

et al. 2014

Urol Int

128

102

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cepted that free radicals play a role in carcinogenesis and that BPH should be considered a premalignant condition which may evolve into prostate cancer. High OS parameters and low antioxidant activity are more prominent in prostate cancer patients compared with BPH and controls. Conclusions: Further studies are needed to clarify the potential role of antioxidants in BPH also in view of preventing the progression to prostate cancer. IntroductionBenign prostatic hyperplasia (BPH) is a prevalent and chronic progressive disease that may be correctly defined as prostate gland enlargement secondary to hyperproliferation of stromal and glandular cells, with predominance of mesenchymal cells [1] . It is an extremely common disease of ageing men and carries a distressingly high morbidity because of its irritative and obstructive symptoms. The etiology and pathogenesis of BPH are not well understood [2] . Key WordsAntioxidants · Benign prostatic hyperplasia · Oxidative stress Abstract Background: Several parameters including inflammatory mediators, hormones, dietary factors, inflammatory genes, and oxidative stress (OS) have been considered to play a role in the development of benign prostatic hyperplasia (BPH). Prostate tissue damage and OS may lead to compensatory cellular proliferation with resulting hyperplastic growth. Methods: We searched MEDLINE for articles in English published up to March 2014 using the key words 'oxidative stress', 'antioxidants' and 'benign prostatic hyperplasia'. Results: Prostatic inflammation can cause the generation of free radicals. The extent of oxidative damage can be exacerbated by a decreased efficiency of antioxidant defense mechanisms. The balance between OS and the antioxidant component also has a role in developing prostate disease. Several works show the role of oxidant products and of depletion of antioxidant substances in BPH patients. It is ac-

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Section: Role Of Depletion Of Antioxidant Activitymentioning

confidence: 99%

Oxidative Stress in Benign Prostatic Hyperplasia: A Systematic Review

Minciullo

Inferrera²,

Navarra³

et al. 2014

Urol Int

128

102

View full text Add to dashboard Cite

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“…Human GSTs can be divided into five main classes of enzymes: alpha, mu, pi, theta, and zeta. Of these, GSTP1 (located on 11q13), GSTT1 (on 22q11.23), and GSTM1 (on 1p13.3) exhibit genetic polymorphisms that may lead to altered enzyme activity, which has been associated with many diseases [25][26][27]. GSTP1 exhibits a polymorphism within its coding region (A to G transition at nucleotide +313, thus changing codon 104 from ATC [Ile] to GTC [Val]), which leads to decreased enzyme activity [28].…”

Section: Gst and Risk Of Gerdmentioning

confidence: 99%

Genetic factors in the pathogenesis of gastroesophageal reflux disease

Ghoshal

Chourasia

2011

Indian J Gastroenterol

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Multiple factors play a role in the pathogenesis of gastroesophageal reflux disease (GERD). Two landmark studies showing higher concordance of disease in monozygotic than dizygotic twin pairs suggested the role of host genetic factors in its pathogenesis. Recent studies have shown that genetic polymorphism in genes influencing host's inflammatory response, drug metabolism, cell cycle regulation, xenobiotic pathways, DNA repair, mutagenesis, esophageal sensory function and gene silencing are associated with risk of GERD and its sequelae-Barrett's esophagus and esophageal adenocarcinoma. However, more studies on larger sample size are needed before reaching a definite conclusion on the role of an individual gene.

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“…However, the exact mechanism by which GST polymorphisms might lead to higher cancer risk is not well understood. Studies also report risk of BPH due to GST polymorphism [15]. Hence, the present pilot study was planned to investigate the association of concomitant deletions of GST genes with a marker of oxidative stress in subjects with BPH or prostate cancer.…”

Section: Discussionmentioning

confidence: 99%

“…Absence of these enzymes due to homozygous deletions are implicated in poor elimination of carcinogenic substances including constituents of tobacco which are potential sources of ROS in our body, making individuals with these deletions susceptible to oxidative injury [10]. Studies have reported positive association of GSTM1 or GSTT1 polymorphism with increased risk of BPH and prostate cancer [11][12][13][14][15]. Since these individual deletions are reported to be associated with increased risk, effect of deletion of both these genes could be additive.…”

Section: Introductionmentioning

confidence: 99%

Association ofGSTM1andGSTT1Polymorphism with Lipid Peroxidation in Benign Prostate Hyperplasia and Prostate Cancer: A Pilot Study

et al. 2011

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Association of glutathione S-transferase (GST) M1 and T1 deletions with benign prostate hyperplasia (BPH) and prostate cancer is well reported. These enzymes metabolize numerous toxins thus protecting from oxidative injury. Oxidative stress has been associated with development of BPH and prostate cancer. The present study was designed to analyze role of GST deletions in development of oxidative stress in these subjects. GSTs are responsible for metabolism of toxins present in tobacco therefore effect of tobacco usage in study groups was also studied. Three groups of subjects: BPH (57 patients), prostate cancer (53 patients) and controls (46 subjects) were recruited. Genotyping was done using a multiplex polymerase chain reaction (PCR) method. Malondialdehyde (MDA) levels as marker of oxidative stress were estimated by measuring thiobarbituric acid reactive substance (TBARS) in plasma. Based on genotyping, subjects were categorized into: GSTM1+/GSTT1+, GSTM1-/GSTT1+, GSTM1+/GSTT1- and GSTM1-/GSTT1-. Significantly higher plasma MDA levels were noticed in GSTM1-/GSTT1- as compared to GSTM1+/GSTT1+ in all study groups. Double deletion (GSTM1-/GSTT1-) is associated with higher oxidative stress which might play a role in the pathogenesis of BPH and prostate cancer. However, other markers of oxidative stress should be analyzed before any firm conclusion.

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GSTM1,GSTM3andGSTT1Gene Variants and Risk of Benign Prostate Hyperplasia in North India

Cited by 11 publications

References 27 publications

Oxidative Stress in Benign Prostatic Hyperplasia: A Systematic Review

Oxidative Stress in Benign Prostatic Hyperplasia: A Systematic Review

Genetic factors in the pathogenesis of gastroesophageal reflux disease

Association ofGSTM1andGSTT1Polymorphism with Lipid Peroxidation in Benign Prostate Hyperplasia and Prostate Cancer: A Pilot Study

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