Reactive Oxygen Spices Scavenging Behavior of Selenium Upon Vinyl Chloride Interaction With Hemoglobin

BackgroundVinyl chloride (VC) a colorless gas with a pleasant odor that is capable of entering the body through oral or inhalation routes. Extensive studies on this compound indicated that it is a carcinogen, and Vinyl chloride exposure can result in a specific type of cancer in VC workers. Whereas hemoglobin plays a vital role in oxygen transfer throughout the body, the effect of VC on human hemoglobin has not been studied in a molecular aspect. Furthermore, selenium as an antioxidant is a vital factor for the health of humans and animals. Therefore, the effect of the antioxidant capability of selenium on the interaction between vinyl chloride and hemoglobin was studied.MethodsThe effect of the antioxidant capability of selenium on the interaction between VC and hemoglobin was investigated by different spectroscopy methods such as UV-visible, Fourier-transform infrared, chemiluminescence, and fluorescence spectroscopies and molecular dockingResultsThe results indicated the destruction of hemoglobin structure in the presence of different concentrations of vinyl chloride, but in the presence of selenium, the damaging effect of VC on hemoglobin structure was decreased, relying on its antioxidant capability results.ConclusionsAccording to our findings, vinyl chloride destroyed hemoglobin structure utilizing ROS production, and the presence of selenium as an antioxidant inhibits the destroying effect of vinyl chloride on hemoglobin

Understanding Benefits of Curcumin on Cognitive Function from Molecular Aspect: A Review

Cognitive function has a significant impact on individuals’ quality of life. Over time, human cognitive function tends to decline. The importance of cognitive function in everyday life has led many researchers to seek alternative treatments to maintain and improve cognitive function. Some studies show that curcumin can improve cognitive function and prevent cognitive decline in humans. This review focuses on the benefits of curcumin on cognitive function and the mechanism of how it works from molecular aspect. According to some studies, one of the factors leading to cognitive decline is chronic low-grade systemic inflammation. This review will focus on antioxidant, anti-inflammatory, neuroprotective effects, and β amyloid aggregation inhibition properties of curcumin that can improve cognitive function or delay cognitive decline. It is important to understand the basic reasons why curcumin can have benefits on cognitive function, this can be seen from the mechanisms that are reflected in the biomolecular aspect.

CB1R regulates soluble leptin receptor levels via CHOP, contributing to hepatic leptin resistance

The soluble isoform of leptin receptor (sOb-R), secreted by the liver, regulates leptin bioavailability and bioactivity. Its reduced levels in diet-induced obesity (DIO) contribute to hyperleptinemia and leptin resistance, effects that are regulated by the endocannabinoid (eCB)/CB1R system. Here we show that pharmacological activation/blockade and genetic overexpression/deletion of hepatic CB1R modulates sOb-R levels and hepatic leptin resistance. Interestingly, peripheral CB1R blockade failed to reverse DIO-induced reduction of sOb-R levels, increased fat mass and dyslipidemia, and hepatic steatosis in mice lacking C/EBP homologous protein (CHOP), whereas direct activation of CB1R in wild-type hepatocytes reduced sOb-R levels in a CHOP-dependent manner. Moreover, CHOP stimulation increased sOb-R expression and release via a direct regulation of its promoter, while CHOP deletion reduced leptin sensitivity. Our findings highlight a novel molecular aspect by which the hepatic eCB/CB1R system is involved in the development of hepatic leptin resistance and in the regulation of sOb-R levels via CHOP.

CB1R Regulates Soluble Leptin Receptor Levels via CHOP, Contributing to Hepatic Leptin Resistance

The soluble isoform of leptin receptor (sOb-R), secreted by the liver, regulates leptin bioavailability and bioactivity. Its reduced levels in diet-induced obesity (DIO) contributes to hyperleptinemia and leptin resistance, effects that are known to be regulated by the endocannabinoid (eCB)/CB1R system. Here we show that pharmacological activation/blockade as well as genetic overexpression/deletion of hepatic CB1R modulates sOb-R levels and consequently hepatic leptin resistance. Interestingly, peripheral CB1R blockade failed to reverse DIO-induced reduction of sOb-R levels, fat mass, dyslipidemia, and hepatic steatosis in mice lacking C/EBP homologous protein (CHOP), whereas direct activation of CB1R in hepatocytes reduced sOb-R levels in a CHOP-dependent manner. Moreover, CHOP stimulation increased sOb-R expression and release via a direct regulation of its promoter, while CHOP deletion reduced leptin sensitivity. Our findings highlight a novel molecular aspect by which the hepatic eCB/CB1R system involves in the development of hepatic leptin resistance by regulating sOb-R levels via CHOP.SummaryHere we describe a novel molecular aspect by which the hepatic endocannabinoid/CB1R system contributes to hepatic leptin resistance by regulating soluble leptin receptor levels via CHOP.