Toxicology International (Formerly Indian Journal of Toxicology)

Suraj Singh Yadav , Manish Kumar Singh , Pradeep Dwivedi , Raju Kumar Mandal , Kauser Usman , Sanjay Khattri , Kamlesh Kumar Pant

Abstract

Introduction: A consortium of metabolic risk factors accelerate the onset of diabetes, heart disease, stroke, and certain cancers. Proteolytic enzymes like matrix metalloproteinases (MMP) are regulated by a group of endogenous proteins called tissue inhibitors of metalloproteinases (TIMP). These TIMPs binds to active and alternate sites of activated MMPs and facilitate regulation. Impaired expression of MMPs may have a significant contribution in the pathogenesis of many tissues-destructive processes like tumor progression and cardiovascular and metabolic disorders. Materials and Methods: This case control study lays stress on the possible role of impaired levels of circulating MMP‑2 and 9 in metabolic syndrome (MetS). The age, sex‑matched 388 subjects with 190 newly diagnosed patients, and 198 healthy controls were recruited. To screen the patients with MetS, biochemical analysis of patients for impaired glucose level, hypertension, body mass index (BMI), and lipid profile was performed. The circulating level of MMP‑2 and ‑9 in serum was analyzed by enzyme‑linked immunosorbent assay (ELISA) in all patients and control. Results: All metabolic risk factors were statistically significant (P < 0.01) in patients against control group. The serum MMP‑2 and ‑9 level was significantly higher (P < 0.001) in patients having MetS as compared with control group. Conclusions: Similar trend was observed in gender wise analysis of serum MMP level. Higher MMP level alteration observed in male patients as compared with female patients.

Keywords

Insulin resistance, metabolic syndrome, matrix metalloproteinases‑2, matrix metalloproteinases‑9

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Shailendra Dwivedi , Apul Goel , Anil Mandhani , Sanjay Khattri , Kamlesh Kumar Pant

Abstract

Prostate cancer is responsible for major deaths globally after lung cancer. However, etiology of prostate cancer is still unknown. Individual risk and incidence of prostate cancer may result from the interaction of genetic susceptibility with exposure to environmental factors such as infectious agents, tobacco, occupational exposure, dietary carcinogens, and/or hormonal imbalances leading to injury of the prostate and to the development of chronic inflammation. About 30% of all human cancers are caused by tobacco smoking and inhaled pollutants. Inflammation is now regarded as an important hallmark of cancer. The present study has been aimed to explore the pro‑inflammatory levels in prostate carcinoma patients by examining the serum levels of novel cytokine interleukin‑18 (IL‑18) expression in tobacco exposed population. A total of 578 (n = 284 biopsy proven prostate cancer patients, n = 294 controls with and without tobacco exposed population) were recruited. Serum IL‑18 (Interleukin‑18) level was done by ELISA. The IL‑18 levels between cancer patients and controls within same mode tobacco exposure as tobacco smoking (overall) showed significant difference (P < 0.0001) and further we compared within stratified group, it significantly differ (P < 0.0001) in bidi and cigarette smoking than control non users. Furthermore, IL‑18 levels in tobacco chewers (overall) with gutkha and khaini chewers showed significant difference (P < 0.01) than controls non users. Moreover, the IL‑18 levels between cancer patients and controls with in of combined mode chewers smokers and alcohol (CSA), smokers with alcohol showed significant difference (P < 0.01) than controls. The IL‑18 levels also differed significantly (P < 0.05) with smokers and chewers in higher stages of III and IV, and showed non significant with in lower stages. Tobacco exposure enhance the inflammation in prostate carcinoma patients in stratified group as it have been represented as a risk factors in various cancers, but this study provide further its role that seems to influence inflammation especially in prostate carcinoma.

Keywords

Interleukin‑18, NF‑KB, prostate cancer, tobacco chewers, tobacco smokers

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