Oxidative stress, a cytopathic outcome of excessive generation of ROS and the repression of antioxidant defense system for ROS elimination, is involved in the pathogenesis of multiple diseases, including diabetes and its complications. Retinopathy, a microvascular complication of diabetes, is the primary cause of acquired blindness in diabetic patients. Oxidative stress has been verified as one critical contributor to the pathogenesis of diabetic retinopathy. Oxidative stress can both contribute to and result from the metabolic abnormalities induced by hyperglycemia, mainly including the increased flux of the polyol pathway and hexosamine pathway, the hyper-activation of protein kinase C (PKC) isoforms, and the accumulation of advanced glycation end products (AGEs). Moreover, the repression of the antioxidant defense system by hyperglycemia-mediated epigenetic modification also leads to the imbalance between the scavenging and production of ROS. Excessive accumulation of ROS induces mitochondrial damage, cellular apoptosis, inflammation, lipid peroxidation, and structural and functional alterations in retina. Therefore, it is important to understand and elucidate the oxidative stress-related mechanisms underlying the progress of diabetic retinopathy. In addition, the abnormalities correlated with oxidative stress provide multiple potential therapeutic targets to develop safe and effective treatments for diabetic retinopathy. Here, we also summarized the main antioxidant therapeutic strategies to control this disease.

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Triclosan (TCS), an extensively used antimicrobial agent, has raised considerable concern due to its hepatocarcinogenic potential. However, previous hepatotoxicity studies primarily focused on the activation of specific intracellular receptors, the underlying mechanisms still warrant further investigation at the metabolic level. Herein, we applied metabolomics in combination with lipidomics to unveil TCS-related metabolic responses in human normal and cancerous hepatocytes. Endogenous and exogenous metabolites were analyzed for the identification of metabolic biomarkers and biotransformation products. In L02 normal cells, TCS exposure induced the up-regulation of purine metabolism and amino acid metabolism, caused lipid accumulation, and disturbed energy metabolism. These metabolic disorders in turn enhanced the overproduction of reactive oxygen species (ROS), leading to the alteration of antioxidant enzyme activities, down-regulation of endogenous antioxidants, and peroxidation of lipids. TCS-induced oxidative stress is thus considered to be one crucial factor for hepatotoxicity. However, in HepG2 cancer cells, TCS underwent fast detoxification through phase II metabolism, accompanied by the enhancement of energy metabolism and elevation of antioxidant defense system, which contributed to the potential effects of TCS on human hepatocellular carcinoma development. These different responses of metabolism between normal and cancerous hepatocytes provide novel and robust perspectives for revealing the mechanisms of TCS-triggered hepatotoxicity.

14Methane production rate (MPR) in waste activated sludge (WAS) digestion processes is typically limited 15 by the initial steps of complex organic matter degradation, leading to a limited MPR due to sludge 16 fermentation speed of solid particles. In this study, a novel microbial electrolysis AD reactor (ME-AD) was 17 used to accelerate methane production for energy recovery from WAS. Carbon bioconversion was 18 accelerated by ME producing H 2 at the cathode. MPR was enhanced to 91.8 gCH 4 /m 3 reactor/d in the 19 microbial electrolysis ME-AD reactor, thus improving the rate by 3 times compared to control conditions 20 (30.6 gCH 4 /m 3 reactor/d in AD). The methane production yield reached 116.2 mg/g VSS in the ME-AD 21 reactor. According to balance calculation on electron transfer and methane yield, the increased methane 22 production was mostly dependent on electron contribution through the ME system. Thus, the use of the 23 novel ME-AD reactor allowed to significantly enhance carbon degradation and methane production from 24 WAS. 25 26 2 29 1. Introduction 30 The large amount of activated sludge generated during wastewater treatment poses a critical threat (when 31 not properly disposed) to ecological systems [1], while proper treatment and disposal of excess sludge is 32 quite expensive (Wei et al. 2003). On the other hand, anaerobic digestion (AD) is widely used for sludge 33 reduction as an energy saving and recovering method [2]. However, AD rate is substantially limited by the 34 first two steps (hydrolysis and acidogenesis) to convert complex organic compounds into suitable substrates 35 for methanogenesis, in raw sludge [3-5]. Commonly, it takes from 20 to 30 days to degrade 30-50% of the 36 total COD or volatile solids (VS) of raw WAS, under mild environmental conditions [6]. The pressure of 37 rapid human population growth and increasing energy demand have thus promoted further research on 38 development and improvement of an rate-accelerating AD process, in order to enhance biogas production 39 and achieve faster degradation rate from WAS [7, 8]. 40Recently, some researchers pointed out that bioelectrochemical systems have the ability to promote carbon 41 oxidation on anode and in-site CO 2 capture and reduction on cathode, thus providing additional CH 4 42 formation in an integrated AD system [9, 10]. Recently a direct interspecies electron transfer for 43 methanogenesis has been proved between Geobacter and Methanosaeta [11]. However, few efforts have 44 been made to better understand bioelectrochemical contributions to organic conversion or methane 45 promotion, which is very important to achieve viable reactor operations in the future. Lately, microbial 46 electrolysis cells (MECs) have been tested for their ability to convert waste organic compounds from 47 3 Therefore, in this study, a coupled system was tested, by putting a microbial electrolysis (ME) system into 59 an AD system, for raw waste activated sludge treatment at mild environmental conditions. The microbial 60 electrolysis system wa...