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Insulin resistance is a significant contributor to the development of type 2 diabetes (T2D) and is associated with obesity, physical inactivity, and low maximal oxygen uptake. While intense and prolonged exercise may have negative effects, physical activity can have a positive influence on cellular metabolism and the immune system. Moderate exercise has been shown to reduce oxidative stress and improve antioxidant status, whereas intense exercise can increase oxidative stress in the short term. The impact of exercise on pro‐inflammatory cytokine production is complex and varies depending on intensity and duration. Exercise can also counteract the harmful effects of ageing and inflamm‐ageing. This review aims to examine the molecular pathways altered by exercise in non‐obese individuals at higher risk of developing T2D, including glucose utilization, lipid metabolism, mitochondrial function, inflammation and oxidative stress, with the potential to improve insulin sensitivity. The focus is on understanding the potential benefits of exercise for improving insulin sensitivity and providing insights for future targeted interventions before onset of disease. [ABSTRACT FROM AUTHOR]

The freshwater fish Carassius auratus was chosen as an experimental subject, and their hepatic biochemical responses to the medium-term exposure of Benzo(k)fluoranthene (BkF) alone and in combination with PCB118 and dichlorodiphenyltrichloroethane (DDT) were investigated by measuring the reduced glutathione (GSH), glutathione S-transferase (GST), and thiobarbituric acid reactive substances (TBARS), to assess sublethal effects. The hepatic GSH content was significantly inhibited by organic pollutants, alone and in mixtures, while the TBARS content was significantly induced after three days of exposure. Bell-shaped concentration-response charts of GST activities were obtained. Significant dose-response relationships were found for hepatic GSH and TBARS contents of all concentrations and for the GST activity, except at the highest concentration. The GSH content, GST activity, and TBARS content in Carassius auratus were confirmed as useful biomarkers of exposure to organic pollutions.

In this report, the effect of hydrogen-rich water (HRW), which was used to investigate the physiological roles of hydrogen gas (H2) in plants recently, on the regulation of plant adaptation to mercury (Hg) toxicity was studied. Firstly, we observed that the exposure of alfalfa seedlings to HgCl2 triggered production of reactive oxygen species (ROS), growth stunt and increased lipid peroxidation. However, such effects could be obviously blocked by HRW. Meanwhile, significant decreases in the relative ion leakage and Hg accumulation were observed. Hg-induced increases in total and isozymatic activities of superoxide dismutase (SOD) were significantly reversed by HRW. Further results suggested that HRW-induced the activities of guaiacol peroxidase (POD) and ascorbate peroxidase (APX), two hydrogen peroxide-scavenging enzymes, was at transcriptional levels. Meanwhile, obvious increases of the ratios of reduced/oxidized glutathione (GSH), homoglutathione (hGSH), and ascorbic acid (AsA) and corresponding gene expression were consistent with the decreased oxidative damage in seedling roots. In summary, the results of this investigation indicated that HRW was able to alleviate Hg toxicity in alfalfa seedlings by (i) alleviating growth stunt and reducing Hg accumulation, and (ii) avoidance of oxidative stress and reestablishment of redox homeostasis. [Copyright &y& Elsevier]

Highlights: [•] HPLC profiling indicated that MEBG contained alliin. [•] MEBG suppressed the body weight in obese rats fed a HFD. [•] MEBG inhibited the liver size, perirenal, and epididymal fat in obese rats. [•] MEBG suppressed the serum lipid profile in obese rats. [•] MEBG decreased the lipogenesis and increased the fatty acid β-oxidation. [Copyright &y& Elsevier]

Highlights: [•] The 24h rhythms under oxidative stress in Drosophila are studied. [•] Abolishment of per mRNA rhythm in H2O2 treated flies was seen. [•] Reversibility of ROS homeostasis rhythms under Bacopa treatment was noticed. [•] Circadian clock is sensitive to oxidative stress, particularly in cryb mutant. [Copyright &y& Elsevier]

Highlights: [•] TCBQ-intoxication elevated ALT, AST activities and TBIL content. [•] TCBQ-intoxication induced necrosis and inflammatory in liver section. [•] TCBQ-intoxication increased ROS, TBARS and decreased antioxidant activities. [•] TCBQ-intoxication induced HO-1 and NQO1 expression. [•] Pretreatment of CGA relieved TCBQ-induced liver damage remarkably. [Copyright &y& Elsevier]

Highlights: [•] Beneficial effect of NHDC on CCl4-induced acute oxidative injury was discussed. [•] NHDC significantly ameliorated oxidative damage in mice liver and serum. [•] NHDC significantly suppressed oxidative damage in HepG2 cells. [•] NHDC is a powerful antioxidant and is a potential hepatoprotective agent. [ABSTRACT FROM AUTHOR]

Abstract: Lotus (Nelumbo Nucifera) root, a well-known medicinal plant in Asia, is reported to have various therapeutic benefits, including anti-diabetes, anti-hypertension, and anti-hyperlipidaemia. We hypothesized that the ethanol extract of lotus root (ELR) would exhibit an anti-adipogenic effect in human pre-adipocytes as well as anti-obesity and anti-oxidant effects in rats fed a high-fat diet. Treatment with ELR in human pre-adipocytes resulted in inhibition of lipid accumulation and attenuated expression of adipogenic transcription factors such as peroxisome proliferator-activated receptor gamma and adipocyte marker genes, such as glucose transporter 4 and leptin. Administration of ELR resulted in a significant decrease in relative weights of adipose tissues in rats fed a high-fat diet. Consumption of a high-fat diet resulted in an increase in serum total cholesterol (TC) and triglyceride (TG) levels; however, administration of ELR resulted in a decrease in the levels of TC and TG. Administration of ELR resulted in a decrease in the level of serum leptin and insulin. Administration of ELR in rats fed a high-fat diet resulted in a decrease in hepatic thiobarbituric acid reactive substance content, elevated by a high-fat diet and an increase in superoxide dismutase activity and hepatic glutathione content. These results suggest that lotus root exerts anti-oxidant and anti-obesity effects and could be used as a functional and nutraceutical ingredient in combatting obesity-related diseases. [Copyright &y& Elsevier]

Highlights: [•] Tributyltin chloride induces oxidative damage in Leydig cells. [•] Cell death is evident which consists of both necrosis and apoptosis. [•] Calcium inhibitors and free radical scavengers show protective efficacy. [•] Exposure to TBTC resulted in disruption of steroidogenic activity. [•] Testosterone release is significantly affected following TBTC exposure. [ABSTRACT FROM AUTHOR]

Highlights: [•] Health effects of bioactive metabolites from dietary polyphenols. [•] Molecular targets of bioactive metabolites from microbiota and faeces. [•] Molecular targets of bioactive metabolites from liver microsomes. [•] Molecular targets of bioactive metabolites from plasma. [•] Molecular targets of bioactive metabolites from urine. [Copyright &y& Elsevier]

Abstract: Sub-acute brain ischemia is a risk factor for the development of vascular dementia (VaD). Sub-acute brain ischemia induced VaD, participates in a negative role in impaired cognition. Imidazoline receptors are widely expressed in the central nervous system. But the role of I1-imidazoline and α2-adrenoceptors in VaD are still unknown. The present study has been designed to investigate the role of selective I1-imidazoline receptor modulator; moxonidine as well as α2-adrenoceptor modulator; clonidine in sub-acute brain ischemia induced VaD in mice (n=8). Permanent bilateral common carotid arteries ligation (2VO) technique was used to induce sub-acute brain ischemia in mice. Assessment of spatial learning and memory was done by using Morris water maze. Brain damage was assessed as percent infarct, using TTC staining of brain coronal sections. Oxidative stress was assessed by estimating brain malondialdehyde (MDA), catalase (CAT), glutathione (GSH) and superoxide dismutase (SOD). Cholinergic status was assessed by brain acetylcholinesterase (AChE) activity. 2VO animals have shown significant reduction in learning and memory as well as brain CAT, GSH and SOD, with significant increase in brain infarct size, MDA and AChE activity. Whereas, administration of moxonidine and clonidine significantly attenuated 2VO induced learning and memory deficits, brain damage, brain oxidative stress and higher AChE activity. It may be concluded that 2VO induced sub-acute brain ischemia has elicited dementia, which was attenuated by moxonidine and clonidine. Thus, modulators of I1-imidazoline receptors may be explored further for their benefits in sub-acute brain ischemia induced vascular dementia. [Copyright &y& Elsevier]

Abstract: The biochemical responses of the enzymatic antioxidant system of a drought-tolerant cultivar (IACSP 94-2094) and a commercial cultivar in Brazil (IACSP 95-5000) grown under two levels of soil water restriction (70% and 30% Soil Available Water Content) were investigated. IACSP 94-2094 exhibited one additional active superoxide dismutase (Cu/Zn-SOD VI) isoenzyme in comparison to IACSP 95-5000, possibly contributing to the heightened response of IACSP 94-2094 to the induced stress. The total glutathione reductase (GR) activity increased substantially in IACSP 94-2094 under conditions of severe water stress; however, the appearance of a new GR isoenzyme and the disappearance of another isoenzyme were found not to be related to the stress response because the cultivars from both treatment groups (control and water restrictions) exhibited identical changes. Catalase (CAT) activity seems to have a more direct role in H2O2 detoxification under water stress condition and the shift in isoenzymes in the tolerant cultivar might have contributed to this response, which may be dependent upon the location where the excessive H2O2 is being produced under stress. The improved performance of IACSP 94-2094 under drought stress was associated with a more efficient antioxidant system response, particularly under conditions of mild stress. [Copyright &y& Elsevier]

Highlights: [•] Rotenone produced PD-like behavioral and neurochemical alterations. [•] Rotenone causes increased oxidative stress and histopathological changes. [•] AESC and AFSC attenuated the rotenone induced behavioral and neurochemical changes. [•] Histopathological and biochemical alterations were also attenuated by AESC and AFSC. [•] AFSC have shown the maximum ameliorative effect against rotenone induced toxicity. [ABSTRACT FROM AUTHOR]

Abstract: Ethnopharmacological relevance: Long term hyperglycemia leads to development of complications associated with diabetes. Diabetic complications are now a global health problem without effective therapeutic approach. Hyperglycemia and oxidative stress are important components for the development of diabetic complications. Over the past few decades, herbal medicines have attracted much attention as potential therapeutic agents in the prevention and treatment of diabetic complications due to their multiple targets and less toxic side effects. This review aims to assess the current available knowledge of medicinal herbs for attenuation and management of diabetic complications and their underlying mechanisms. Material and methods: Bibliographic investigation was carried out by scrutinizing classical text books and peer reviewed papers, consulting worldwide accepted scientific databases (SCOPUS, PUBMED, SCIELO, NISCAIR, Google Scholar) to retrieve available published literature. The inclusion criteria for the selection of plants were based upon all medicinal herbs and their active compounds with attributed potentials in relieving diabetic complications. Moreover, plants which have potential effect in ameliorating oxidative stress in diabetic animals have been included. Results: Overall, 238 articles were reviewed for plant literature and out of the reviewed literature, 127 articles were selected for the study. Various medicinal plants/plant extracts containing flavonoids, alkaloids, phenolic compounds, terpenoids, saponins and phytosterol type chemical constituents were found to be effective in the management of diabetic complications. This effect might be attributed to amelioration of persistent hyperglycemia, oxidative stress and modulation of various metabolic pathways involved in the pathogenesis of diabetic complications. Conclusion: Screening chemical candidate from herbal medicine might be a promising approach for new drug discovery to treat the diabetic complications. There is still a dire need to explore the mechanism of action of various plant extracts and their toxicity profile and to determine their role in therapy of diabetic complications. Moreover, a perfect rodent model which completely mimics human diabetic complications should be developed. [Copyright &y& Elsevier]

Abstract: Pu-Erh tea (PET) is a fully fermented tea cultivated in the Yunnan Province of China. It is widely appreciated and consumed as the healthful beverage. In vivo, in vitro and clinical studies have suggested the health benefits of PET for a variety of hypolipidemic, antiobesity, antimutagenic, antioxidative, antitumor, free radical scavenging and toxicity suppressing activities. Many of these beneficial impacts are related to its bioactive compounds, particularly theabrownin and gallic acid. However, there are some scientific evidences underlying the risk of pathological abnormalities associated with the high doses of PET extracts. Confirming the assertion, this paper presents a state of art review of PET, its tasting, sensory evaluation and aroma characterization. The key advances of its wide implications in the adsorption engineering, toxicological, pharmacological and medical science development are laconically elucidated. Furthermore, the challenges and future prospects for the integration of PET practice are outlined. [Copyright &y& Elsevier]

Highlights: [•] Puerarin protects against structural hepatic damageinducedby CCl4. [•] Puerarin increased the activities of SOD, CAT, GPx, and GR in CCl4-treated liver. [•] Puerarin reduced the lipid peroxidation inducedby CCl4 treatment. [•] Puerarin is a potential natural product to treat chemical-induced hepatotoxicity. [ABSTRACT FROM AUTHOR]

Highlights: [•] Oleanolic acid (OA) improves hepatic insulin resistance in db/db mice. [•] OA inhibits mitochondrial oxidative stress via activation of Nrf2–GCLc signal. [•] OA suppresses hepatic lipid accumulation and inflammation. [Copyright &y& Elsevier]

β-Thalassemia (β-thal) is associated with abnormal synthesis of hemoglobin (Hb). Repeated blood transfusions in patients with β-thal major (β-TM) leads to an enhanced generation of reactive oxygen species (ROS), and subjects patients to peroxidative injury. We studied the antioxidant status and oxidative damage to children with β-thal in Jordan. Samples from 40 children with β-thal and 40 healthy controls were used. All children were under 13 years of age. Our results showed that plasma thiobarbituric acid reactive substances (TBARS) were elevated in β-thalassemic children compared to controls together with compensatory increase in superoxide dismutase (SOD) activity and decrease in catalase (CAT) activity. Elevated serum ferritin showed positive correlation with elevated liver enzyme levels except gamma glutamyl transferase (GGT), confirming liver involvement due to iron overload. Serum ferritin also showed a positive correlation with elevated TBARS and SOD, suggesting that iron overload is involed in the oxidative stress shown in cells. [ABSTRACT FROM AUTHOR]

Abstract: It is generally accepted that copper toxicity is a consequence of the generation of reactive oxygen species (ROS) by copper ions via Fenton or Haber–Weiss reactions. Copper ions display high affinity for thiol and amino groups occurring in proteins. Thus, specialized proteins containing clusters of these groups transport and store copper ions, hampering their potential toxicity. This mechanism, however, may be overwhelmed under copper overloading conditions, in which copper ions may bind to thiol groups occurring in proteins non-related to copper metabolism. In this study, we propose that indiscriminate copper binding may lead to damaging consequences to protein structure, modifying their biological functions. Therefore, we treated liver subcellular membrane fractions, including microsomes, with Cu2+ ions either alone or in the presence of ascorbate (Cu2+/ascorbate); we then assayed both copper-binding to membranes, and microsomal cytochrome P450 oxidative system and GSH-transferase activities. All assayed sub-cellular membrane fractions treated with Cu2+ alone displayed Cu2+-binding, which was significantly increased in the presence of Zn2+, Hg2+, Cd2+, Ag+1 and As3+. Treatment of microsomes with Cu2+ in the μM range decreased the microsomal thiol content; in the presence of ascorbate, Cu2+ added in the nM concentrations range induced a significant microsomal lipoperoxidation; noteworthy, increasing Cu2+ concentration to ≥50μM led to non-detectable lipoperoxidation levels. On the other hand, μM Cu2+ led to the inhibition of the enzymatic activities tested to the same extent in either presence or absence of ascorbate. We discuss the possible significance of indiscriminate copper binding to thiol proteins as a possible mechanism underlying copper-induced toxicity. [Copyright &y& Elsevier]

Styrene 7,8-oxide (SO) is the main metabolite of styrene, a neurotoxic compound used industrially. Neurons exposed to SO undergo apoptosis with characteristic features including chromatin rearrangements and caspase activation. We report that the execution phase of apoptosis induced by SO (0.3 mM) in SK-N-MC neurons is triggered by translocation of apoptogenic factors (e.g., cytochrome c) into the cytosol. In addition, mitochondria exhibit lower Ca2+ capacity and loss of mitochondrial membrane potential (ΔΨ). Lipid peroxidation, measured as thiobarbituric acid reactive substances (TBARS), is increased after 12 h. Pre-treatment with the antioxidant MnTBAP (100 μM) prevents the decrease of Ca2+ capacity, cytochrome c release, activation of caspases, exposure of phosphatidylserine and cell death. Hence, the neurotoxic effects of SO are related to mitochondrial damage and oxidative stress. [Copyright &y& Elsevier]

Understanding the effects of prooxidants on mammalian testis either in vitro or in vivo is important, since recent evidence shows that oxidative stress can play a vital role in the etiology of male infertility. In this investigation, we have examined the oxidative stress response of adult rat testis in vitro as induced by model prooxidants (tert-butyl hydroperoxide (t-bHP) and cumene hydroperoxide (cHP) deploying two models—testicular cell suspensions (TCS) and testicular explants (TE). Significant induction of oxidative stress was observed in both models as evidenced by increased thiobarbituric acid reactive substances (TBARS) levels on incubation with hydroperoxides. The response was both concentration and time dependent. At the highest concentration (200 μm), both hydroperoxides induced a 100% increase in the TE model, compared with a dramatic (380–560%) increase in the TCS model during a 30-min incubation. Further evidence of oxidative stress such as reduction in the GSH levels and alterations in the activity of antioxidant enzymes (catalase and glutathione peroxidase) were also obtained in the TE model. In the TE model, radical scavengers, namely thiourea, urea and mannitol, as well as antioxidants such as glutathione and catalase inhibited the t-bHP-induced lipid peroxidation response to varying degree. A similar degree of protection was also evident with known antioxidants such as ascorbic acid, butylated hydroxyanisole and butylated hydroxytoluene in the TE model. Further co-incubation of TE either with mercaptosuccinate (a potent glutathione peroxidase inhibitor) or 3-aminotriazole (an irreversible catalase inhibitor) resulted in a marked increase in t-bHP-induced lipid peroxidation, clearly suggesting the importance of both of these enzymic antioxidants in rat testis in vitro. These data suggest that the TE model may be further utilized to screen antioxidants in vitro and also investigate the prooxidant potency of xenobiotics in testicular cells. [ABSTRACT FROM AUTHOR]

Oxidative stress is seen in various metabolic disorders for unknown reasons. Oxidative stress is defined as an imbalance between pro-oxidant and antioxidant status in favor of the former. This study investigated whether oxidative stress exists in phenylketonuria (PKU) using the BTBR-Pahenu2 animal model for PKU. Animals (14–24 weeks old) were sacrificed and brain and red blood cells (RBCs) were obtained aseptically. The lipid peroxidation by-product, evaluated as malondialdehyde (MDA), was significantly higher in the brains and RBCs of PKU animals (n = 6) than in controls (n = 6). Glutathione/glutathione disulfide, a good indicator for tissue thiol status, was significantly decreased both in the brains and RBCs. Some antioxidant enzymes were also analyzed in RBCs, including glucose-6-phosphate dehydrogenase (G6PD), which provides the RBC’s main reducing power, reduced nicotinamide adenine dinucleotide phosphate (NADPH), and catalase detoxifies H2O2 by catalyzing its reduction to O2 and H2O. Both catalase and G6PD were significantly increased in the RBCs of PKU animals. [Copyright &y& Elsevier]

Aluminium (Al), has the potential to be neurotoxic in humans and animals, and is present in many manufactured foods and medicines and is also added to drinking water for purification purposes. Our previous study demonstrated that chronic Al exposure induced deficits of both long-term potentiation (LTP) and long-term depression (LTD) of excitatory postsynaptic potential (EPSP) and population spike (PS) in rat dentate gyrus (DG) of hippocampus in vivo (Wang et al., 2001). The purpose of the present study was to investigate whether the Al-induced impairment of synaptic plasticity could be reversed by dietary supplementation with vitamin E (Vit E; α-tocopherol). Neonatal Wistar rats were exposed to Al from parturition throughout life by drinking 0.3% aluminium chloride (AlCl3) solution or a diet supplemented with Vit E at 500 μg/g/day with 0.3% AlCl3. The input/output (I/O) function, EPSP and PS were measured in DG area of adult rats (80–100 days of age) in response to stimulation applied to the lateral perforant path. The results showed that: (1) chronic Al exposure reduced the amplitudes of both EPSP LTP (control: 130.4±3%, n=7; Al-exposed: 110±2%, n=9, P<0.001) and PS LTP (control: 241±19%, n=7; Al-exposed: 130±7%, n=9, P<0.001) significantly. Vit E had no significant effects on the Al-induced deficits of EPSP LTP (Al-exposed: 110±2%, n=9; Al-exposed+Vit E: 112±2%, n=8, P>0.05) and PS LTP (Al-exposed: 130±7%, n=9; Al-exposed+Vit E: 129±4%, n=8; P>0.05); (2) the amplitudes of EPSP LTD (control: 84±4%, n=7; Al-exposed: 92±7%, n=9, P<0.01) and PS LTD (control: 81±4%, n=7; Al-exposed: 98±5%, n=9, P<0.001) were also decreased by Al treatment. The impaired EPSP LTD (Al-exposed: 92±7%, n=9; Al-exposed+Vit E: 93±4%, n=8, P>0.05) and PS LTD (Al-exposed: 98±5%, n=9; Al-exposed+Vit E: 94±6%, n=8, P>0.05) were also not significantly affected by Vit E treatment. It was suggested that dietary supplementation with Vit E did not reverse the impairment of synaptic plasticity induced by Al in DG in vivo. [ABSTRACT FROM AUTHOR]

We evaluated the antioxidant status, namely cellular lipid peroxidation, by measuring thiobarbituric acid reactive substances (TBARS), cellular reduced glutathione (GSH) content, glutathione reductase (GSSG-R), glutathione transferase (GST), glutathione peroxidase (GSH-Px) and catalase activities in rat liver, hepatocytes immediately after isolation and in two-dimensional (2D) culture (on non-coated or collagen-coated dishes, as collagen–collagen or collagen–Matrigel sandwich cultures) or three-dimensional (3D) culture on Matrigel-coated dishes. Microsomal cytochrome P450 (CYP)- and UDP-glucuronosyl transferase (UGT)- dependent activities were also assessed in rat livers and hepatocyte cultures. The overall antioxidant status of rat hepatocytes immediately after isolation was not significantly different from that of rat livers. During culture, GSH was increased in 2D but not in 3D cultures in accordance with morphological observations; that is that matrix–cell interactions involving GSH, important in 2D, are minimal in 3D cultures. While UGT- and GST-dependent activities were equivalent in cultured hepatocytes and in rat livers, both catalase and GSH-Px activities decreased with time in all culture configurations. Constitutive CYP-dependent activities were drastically decreased in hepatocytes after isolation and attachment and did not recover in any culture configuration tested. Our results highlight that, although 2D sandwich cultures and 3D cultures on Matrigel allow longevity of rat hepatocyte cultures and optimal induction of CYPs, an imbalance in phase I/phase II detoxication processes in cultured rat hepatocytes occurs, whatever the culture configuration. [ABSTRACT FROM AUTHOR]