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It has been revealed that certain organochlorine pesticides may increase the risk of gastric cancer incidence among farm workers. This research aimed to assay levels of 7 different organochlorine pesticides in the serum of functional dyspepsia, intestinal metaplasia and gastric cancer patients, along with measuring oxidative stress parameters compared to the control group and their associations. The levels of organochlorine pesticides in the serum of gastric cancer (n = 34), intestinal metaplasia (n = 8), functional dyspepsia patients (n = 48) and control group (n = 46), were measured by gas chromatography equipment. Oxidative stress parameters and erythrocyte acetylcholine esterase activity were also measured in these individuals. The levels of some organochlorine pesticides in the serum of gastric cancer patients were significantly higher than those in the control group. Moreover, the profiles of organochlorine pesticide concentrations were different in gastric cancer, intestinal metaplasia and functional dyspepsia patients. Overall, oxidant parameters were significantly higher in gastric cancer and intestinal metaplasia patients than those in functional dyspepsia patients and the control group, except in the case of malondialdehyde. The antioxidant and acetylcholine esterase enzyme activities were significantly higher in the control group than in other groups. Our results showed that progression from functional dyspepsia towards intestinal metaplasia and gastric cancer was associated with elevations in organochlorine pesticide serum levels, which had an association with the induction of oxidative stress and the reduction of antioxidant and acetylcholine esterase enzyme activities.

Background: Type2 Diabetes (T2D) remains one of the most important causes of cardiovascular diseases (CVD). Menopause leads to an increase in CVD and metabolic syndrome, which indicates the role of sex steroids as a protective factor. In the present study, we surveyed the effects of 17β-estradiol (E2) alone and in combination with progesterone (P4) on cardiovascular dysfunction in T2D. Methods: Female ovariectomized (OVX) diabetic rats were divided into eight groups: Sham-Control, Diabetes (Dia), OVX + Dia, OVX + Dia + Vehicle, OVX + Dia + E2, OVX + Dia + P4, OVX + Dia + E2+P4, and OVX + Dia + E2+Vehicle. T2D was induced by a high-fat diet and streptozotocin. E2 and P4 were administrated every four days for four weeks. The heart cytokines and angiotensin II, lipid profile, insulin, water, and food intake and cardiovascular indices were measured. Results: Results showed that single treatment with E2 decreased fasting blood glucose, water, and food intake, atherogenic and cardiac risk indices, and blood pressure. Also, P4 led to a decrease in atherogenic and cardiac risk indices. TNFα and IL-6 levels were increased and IL-10 was decreased in the Dia group, while E2 alone was able to inhibit these changes. The combined use of E2 and P4 eliminated the beneficial effects of E2 on these indices. Although diabetes results in an increment of cholesterol, LDL and triglyceride, hormone therapy with E2 was associated with improved dyslipidemia. Conclusion: The use of E2 alone, and not the individual use of P4, and its combination with E2 improved cardiovascular function in OVX diabetic animals, possibly by reducing the amount of inflammatory cytokines and improving metabolic parameters.

Protective effects of estrogen (E2) on traumatic brain injury (TBI) have been determined. In this study, the hepatoprotective effects of E2 after TBI through its receptors and oxidative stress regulation have been evaluated. Diffuse TBI induced by the Marmarou method in male rats. G15, PHTPP, MPP, and ICI182–780 as selective antagonists of E2 were injected before TBI. The results indicated that TBI induces a significant increase in liver enzymes [Alkaline phosphatase (ALP), Aspartate aminotransferase (AST), Alanine aminotransferase (ALT), Glutamyl transferase (GGT)], and oxidants levels [Malondialdehyde (MDA), Nitric oxide (NO)] and decreases in antioxidant biomarkers [Glutathione peroxidase (GPx) and Superoxide dismutase (SOD)] in the brain and liver, and plasma. We also found that E2 significantly preserved levels of these biomarkers and enzymatic activity. All antagonists inhibited the effects of E2 on increasing SOD and GPx. Also, the effects of E2 on brain MDA levels were inhibited by all antagonists, but in the liver, only ICI + G15 + E2 + TBI group was affected. The impacts of E2 on brain and liver and plasma NO levels were inhibited by all antagonists. The current findings demonstrated that E2 probably improved liver injury after TBI by modulating oxidative stress. Also, both classic (ERβ, ERα) and non-classic [G protein-coupled estrogen receptor (GPER)] receptors are affected in the protective effects of E2.