The effects of green tea (–)‐epigallocatechin‐3‐gallate on reactive oxygen species in 3T3‐L1 preadipocytes and adipocytes depend on the glutathione and 67 kDa laminin receptor pathways

Abstract

Green tea (-)-epigallocatechin-3-gallate (EGCG) is known as to regulate obesity and fat cell activity. However, little information is known about the effects of EGCG on oxidative reactive oxygen species (ROS) of fat cells. Using 3T3-L1 preadipocytes and adipocytes, we found that EGCG increased ROS production in dose- and time-dependent manners. The concentration of EGCG that increased ROS levels by 180-500% was approximately 50 muM for a range of 8-16 h of treatment. In contrast, EGCG dose- and time-dependently decreased the amount of intracellular glutathione (GSH) levels. EGCG was more effective than (-)-epicatechin, (-)-epicatechin-3-gallate, and (-)-epigallocatechin in changing ROS and GSH levels. This suggests a catechin-specific effect. To further examine the relation of GSH to ROS as altered by EGCG, we observed that exposure of preadipocytes and adipocytes to N-acetyl-L-cysteine (a GSH precursor) blocked the EGCG-induced increases in ROS levels and decreases in GSH levels. These observations suggest a GSH-dependent effect of EGCG on ROS production. While EGCG was demonstrated to alter levels of ROS and GSH, its signaling was altered by an EGCG receptor (the so-called 67 kDa laminin receptor(67LR)) antiserum, but not by normal rabbit serum. These data suggest that EGCG mediates GSH and ROS levels via the 67LR pathway.

Green Tea Polyphenols Precondition against Cell Death Induced by Oxygen-Glucose Deprivation via Stimulation of Laminin Receptor, Generation of Reactive Oxygen Species, and Activation of Protein Kinase Cϵ

“…It is intriguing that prion protein also induces intracellular ROS production via NADPH oxidase (71). It has also previously been reported that a high concentration (50 M) of EGCG induced generation of lethal levels of ROS dependent on 67LR (72). It is important to distinguish this previous study from ours.…”

Sugiol inhibits STAT3 activity via regulation of transketolase and ROS-mediated ERK activation in DU145 prostate carcinoma cells

“…Therefore, we hypothesized that sugiol would induce ROS production. Many prior studies reported that natural compounds induce intracellular ROS to kill cancer cells [14][15][16]. Therefore, we investigated whether sugiol induced ROS generation in DU145 cells.…”

“…The high ROS levels in cancer cells renders these cells more susceptible to oxidative stress-induced cell death, which can be exploited for selective cancer therapy [13]. Many known natural compounds, such as curcumin, EGCG, and resveratrol, generate ROS to destroy cancer cells [14][15][16].…”

Role of nuclear factor (erythroid-derived 2)-like 2 in metabolic homeostasis and insulin action: A novel opportunity for diabetes treatment?

“…Notably, resveratrol, curcumin and epigallocatechin-3-gallate are all reported to act as insulin sensitizing agents, reverse hyperglycemia, hyperlipidemia and other symptoms linked to obesity [87][88][89][90] . These natural compounds may initially cause a depolarization of mitochondrial membrane potential and ROS production, then activate the Nrf2 system to exert subsequent protective responses [19,[91][92][93] . Furthermore, these plant-derived polyphenols are electrophilic and can modulate the reactive cysteine residues in Keap1 molecules, leading to a dissociation of Nrf2 from the Nrf2-Keap complex and increasing the free Nrf2 level [94,95] .…”