Effects of thiol antioxidant β-mercaptoethanol on diet-induced obese mice

Abstract

Aims Obesity and insulin resistance are associated with increased oxidant stress. However, treatments of obese subjects with different types of antioxidants often give mixed outcomes. In this work, we sought to determine if long-term supplementation of a thiol antioxidant, β-mercaptoethanol, to diet-induced obese mice may improve their health conditions. Main Methods Middle-age mice with pre-existing diet-induced obesity were provided with low concentration β-mercaptoethanol (BME) in drinking water for six months. Animals were assessed for body composition, gripping strength, spontaneous physical and metabolic activities, as well as insulin and pyruvate tolerance tests. Markers of inflammation were assessed in plasma, fat tissue, and liver. Key findings BME-treated mice gained less fat mass and more lean mass than the control animals. They also showed increased nocturnal locomotion and respiration, as well as greater gripping strength. BME reduced plasma lipid peroxidation, decreased abdominal fat tissue inflammation, reduced fat infiltration into muscle and liver, and reduced liver and plasma C-reactive protein. However, BME was found to desensitize insulin signaling in vivo, an effect also confirmed by in vitro experiments. Conclusion Long-term supplementation of low dose thiol antioxidant BME improved functional outcomes in animals with pre-existing obesity. Additional studies are needed to address the treatment impact on insulin sensitivity if a therapeutic value is to be explored.

Synthetic β‐nitrostyrene derivative CYT‐Rx20 as inhibitor of oral cancer cell proliferation and tumor growth through glutathione suppression and reactive oxygen species induction

“…Because NAC was able to rescue oral cancer cell death induced by CYT‐Rx20, we tested whether two other thiol antioxidants, GSH and 2‐ME, had similar activity . Our results showed that CYT‐Rx20‐induced cytotoxicity was rescued in the presence of either GSH or 2‐ME (Figure A).…”

Activation of Epstein–Barr Virus’ Lytic Cycle in Nasopharyngeal Carcinoma Cells by NEO212, a Conjugate of Perillyl Alcohol and Temozolomide

“…A role for ROS was further confirmed with the use of hydrogen peroxide (H2O2), an ROS-generating molecule [51]. The cells treated with H2O2 responded with an increased expression of CHOP, Zta, Ea-D, and cleaved caspase 3 (Figure 8A).…”

“…We investigated the potential role of ROS by including anti-oxidant compounds to suppress ROS production. C666.1 cells were treated with NEO212 in the presence or absence of ascorbic acid (AA) and beta-mercaptoethanol (BME), two well-known ROS scavengers [ 50 , 51 ]. Figure 8 A,B shows that NEO212 was neither able to potently stimulate CHOP expression nor trigger the lytic cycle when AA or BME were present in the cell culture medium, indicating the requirement of ROS for these processes.…”

3’-hydroxy-4’-methoxy-β-methyl-β-nitrostyrene inhibits tumorigenesis in colorectal cancer cells through ROS-mediated DNA damage and mitochondrial dysfunction

“…However, pretreatment with p38 inhibitor SB203580 showed no significant effects ( Supplementary Figure 1D ). As NAC is a thiol antioxidant, we carried out further cytotoxicity experiments with the use of glutathione (GSH) and 2-mercaptoethanol (2-ME), two other thiol antioxidants [ 17 , 18 ], and the results showed that CYT-Rx20-induced cytotoxicity was largely reversed in the presence of either GSH or 2-ME ( Supplementary Figure 1E ).…”