Yuming Yang,†,§ Qiang Zhao,‡,§ Wei Feng,† and Fuyou Li*,† †Department of Chemistry and State Key Laboratory of Molecular Engineering of Polymers and Institutes of Biomedical Sciences, Fudan University, Shanghai 200433, P. R. China ‡Key Laboratory for Organic Electronics and Information Displays (KLOEID) and Institute of Advanced Materials (IAM), Nanjing University of Posts and Telecommunications, Nanjing 210046, P. R. China.

Luminescent chemodosimeters for bioimaging.

Polyphenols are wide variety of compounds that occur in fruits and vegetables, wine, tea, extra virgin olive oil, chocolate and other cocoa products. Several polyphenols have been demonstrated to have clear antioxidant properties in vitro, and many of their biological actions have been attributed to their intrinsic reducing capabilities. However, this concept appears now to be a simplistic way to conceive their activity. Evidence is indeed accumulating that polyphenols might exert several other specific biological effects that are as yet poorly understood. In this article we review the most recent data on the subject and describe the additional functions that polyphenols can have in biological systems, focusing on their effects on glutathione and its related enzymes. Experimental data indicate that polyhenols may offer an indirect protection by activating endogenous defense systems. Several lines of evidence suggest a tight connection between exogenous and endogenous antioxidants that appear to act in a coordinated fashion. It is reasonable to hypothesize that this is achieved, at least in part, through antioxidant responsive elements (AREs) present in the promoter regions of many of the genes inducible by oxidative and chemical stress. The latest studies strongly suggest that dietary polyphenols can stimulate antioxidant transcription and detoxification defense systems through ARE.

Novel mechanisms of natural antioxidant compounds in biological systems: involvement of glutathione and glutathione-related enzymes.

The fact that aluminium (Al) and lead (Pb) are both toxic metals to living organisms, including human beings, was discovered a long time ago. Even when Al and Pb can reach and accumulate in almost every organ in the human body, the central nervous system is a particular target of the deleterious effects of both metals. Select human population can be at risk of Al neurotoxicity, and Al is proposed to be involved in the etiology of neurodegenerative diseases. Pb is a widespread environmental hazard, and the neurotoxic effects of Pb are a major public health concern. In spite of the numerous efforts and the accumulating evidence in this area of research, the mechanisms of Al and Pb neurotoxicity are still not completely elucidated. This review will particularly address the involvement of oxidative stress, membrane biophysics alterations, deregulation of cell signaling, and the impairment of neurotransmission as key aspects involved Al and Pb neurotoxicity.

Aluminium and lead: molecular mechanisms of brain toxicity

Use of human-derived liver cell lines for the detection of environmental and dietary genotoxicants; current state of knowledge.

Use of a human-derived liver cell line for the detection of cytoprotective, antigenotoxic and cogenotoxic agents.

Tea catechins protect against lead-induced cytotoxicity, lipid peroxidation, and membrane fluidity in HepG2 cells.

Recent studies have shown that lead causes oxidative stress by inducing the generation of reactive oxygen species (ROS) and reducing the antioxidant defense system of cells, which suggests that ant

Tea catechins protect against lead-induced ROS formation, mitochondrial dysfunction, and calcium dysregulation in PC12 cells.

Our previous research showed that tea catechins could significantly increase the viability of lead-exposed PC12 cells. Whereas the cellular thiol status is known to be responsible for protecting against lead-induced toxicity, whether the role of tea catechins on lead-induced PC12 cell toxicity is related to the metabolism of intracellular thiol compounds remained vague. In the present study, it was found that Pb(2+) significantly decreased reduced glutathione (GSH)/oxidative glutathione (GSSG) and protein sulfhydryl groups (PSH)/glutathione-protein mixed disulfide (GSSP) ratios as well as glutathione reductase activities in a concentration-dependent manner. Both (-)-epicatechin and (-)-epicatechin gallate (ECG) supplementation resulted in an increased GSH/GSSG ratio and glutathione reductase activities. The galloylated catechins (ECG or (-)-epigallocatechin gallate) treatment significantly decreased the GSSP levels and increased the intracellular PSH/GSSP ratio in lead-exposed PC12 cells. To our surprise, as compared with the group treated by lead acetate, 100 microM EGC treatment following lead exposure significantly decreased GSH/GSSG and PSH/GSSP ratios, as well as glutathione reductase activities. The results suggested that the effect of tea catechins on the intracellular thiols status in PC12 cells was different, which may be related to their chemical structures and/or regulation of special gene expression properties.

Xianqiang Yang

Papers

Tea catechins protect against lead-induced cytotoxicity, lipid peroxidation, and membrane fluidity in HepG2 cells.

Tea catechins protect against lead-induced ROS formation, mitochondrial dysfunction, and calcium dysregulation in PC12 cells.

Effect of tea catechins on the change of glutathione levels caused by Pb(++) in PC12 cells.