Plastic compounds and liver diseases: Whether bisphenol A is the only culprit.

Plastics, while providing modern conveniences, have become an inescapable source of global concern due to their role in environmental pollution. Particularly, the focus on bisphenol A (BPA) reveals its biohazardous nature and association with liver issues, specifically steatosis. However, research indicates that BPA is just one facet of the problem, as other bisphenol analogues, microplastics, nanoplastics and additional plastic derivatives also pose potential risks. Notably, BPA is implicated in every stage of non-alcoholic fatty liver disease (NAFLD) onset and progression, surpassing hepatitis B virus as a primary cause of chronic liver disease worldwide. As plastic contamination tops the environmental contaminants list, urgent action is needed to assess causative factors and mitigate their impact. This review delves into the molecular disruptions linking plastic pollutant exposure to liver diseases, emphasizing the broader connection between plastics and the rising prevalence of NAFLD.

Correlation between soluble receptor for advanced glycation end products levels and coronary artery disease in postmenopausal nondiabetic women.

BACKGROUND: The established cardiovascular risk factors cannot explain the overall risk of coronary artery disease (CAD), especially in women. Therefore, there is a growing need for the assessment of novel biomarkers to identify women at risk. The receptor for advanced glycation end products (RAGE) and its interaction with the advanced glycation end product (AGE) ligand have been associated with atherogenesis. The soluble fraction of RAGE (sRAGE) antagonizes RAGE signaling and exerts an antiatherogenic effect. AIM: The study aim was to explore the association between plasma levels of sRAGE and CAD in nondiabetic postmenopausal women. METHODS: This case-control study included 110 nondiabetic postmenopausal women who were enrolled in two groups. Group I included 55 angiographically proven CAD subjects with > 50% stenosis in at least one of the major coronary arteries and Group II included 55 healthy control women who did not have CAD or had < 50% stenosis of the coronary arteries. Stenosis was confirmed by invasive angiography. Plasma sRAGE was determined by an enzyme-linked immunosorbent assay. RESULTS: We observed significantly lower plasma sRAGE concentrations in subjects with CAD vs healthy controls (P < 0.05). Univariate and multivariate logistic regression analysis also revealed a significant correlation between plasma sRAGE levels and CAD (P = 0.01). Multivariate odds ratios for CAD revealed that subjects with sRAGE concentrations below 225 pg/mL (lowest quartile) had a 6-fold increase in CAD prevalence independent of other risk factors. CONCLUSION: Our findings indicated that low sRAGE levels were independently associated with CAD in nondiabetic postmenopausal women. Risk assessment of CAD in postmenopausal women can be improved by including sRAGE along with other risk factors.

Analysis of traditional and emerging risk factors in premenopausal women with coronary artery disease: A pilot-scale study from North India.

Premenopausal women are known to have less heart disease than their menopausal counterparts and men. However, there is a rising prevalence of coronary artery disease (CAD) in premenopausal females, which necessitates determination of risk factors that negate the effects of hormonal protection. There are few studies describing the prevalence of traditional and emerging risk factors in premenopausal women with CAD. Thus, our objective was to explore the prevalence of traditional and emerging risk factors and features of coronary lesions in premenopausal women with CAD in an Indian population. Forty premenopausal female patients with angiographically proven CAD and undergoing treatment with conventional therapies and 40 age-matched premenopausal females without any evidence of CAD were enrolled. Premenopausal females with CAD most commonly had the single-vessel CAD and the left anterior descending artery was most commonly involved. The prevalence of hypertension, diabetes, obesity, metabolic syndrome, family history of CAD and 10-year risk score was higher in premenopausal females with CAD than controls. Even after treatment with conventional therapies, premenopausal women with CAD had dyslipidemia and significantly elevated levels of emerging risk factors such as ApoB, ApoB/ApoA1 ratio, hsCRP, lipoprotein (a), uric acid, T4, fibrinogen, and total leukocyte count as compared to controls (p < 0.05). Further, they had significantly lower levels of HDL-C, and Apolipoprotein A1 and T3 which are protective markers for vascular risk. Multivariate regression analysis demonstrated that low levels of Apo A1 and high levels of fibrinogen, hsCRP and TG drive the vascular risk, and therefore these factors should be considered as candidates for better diagnosis, early detection, and intervention of CAD in premenopausal women.

Role of 8-iso-prostaglandin F2alpha and 25-hydroxycholesterol in the pathophysiology of endometriosis.

OBJECTIVE: To investigate the involvement of 8-iso-PGF(2alpha) and 25-hydroxycholesterol (25-OH-Chol) in the pathophysiology of endometriosis. DESIGN: Observational case-control study using enzyme immunoassay and high-performance liquid chromatography (HPLC). SETTING: Postgraduate Institute of Medical Education and Research. PATIENT(S): Forty-five women undergoing laparoscopy (n = 25), laparotomy (n = 19), or tubal ligation (n =1). INTERVENTION(S): Venipuncture and laparoscopic peritoneal fluid (PF) collection. MAIN OUTCOME MEASURE(S): The levels of 8-iso-PGF(2alpha) were determined both in urine and PF of all the patients using enzyme immunoassay. The levels of 25-OH-Chol were determined by using reversed phase HPLC both in the plasma and PF samples. Oxidative damage to DNA was assessed by agarose gel electrophoresis. RESULT(S): Significantly increased levels of 8-iso-PGF(2alpha) were observed both in urine and PF of women with endometriosis compared with control women. Similarly, higher levels of 25-OH-Chol were observed both in plasma and PF of patients compared with controls and the difference was statistically significant. A clear-cut tailing pattern was observed in DNA of patients with endometriosis, indicating significant DNA damage. CONCLUSION(S): Our observations implicate oxidative stress in the pathophysiology of endometriosis. For the first time, we demonstrate that 8-iso-PGF(2alpha) and oxysterols (the known promoters of steroidogenesis) might be the culprits in this disease.