Search

Scientific information on the potential harmful effects of silver nanoparticles (AgNPs) on human health severely lags behind their exponentially growing applications in consumer products. In assessing the toxic risk of AgNP usage, liver, as a detoxifying organ, is particularly important. The aim of this study was to explore the toxicity mechanisms of nano and ionic forms of silver on human hepatoblastoma (HepG2) cells. The results showed that silver ions and citrate-coated AgNPs reduced cell viability in a dose-dependent manner. The IC50 values of silver ions and citrate-coated AgNPs were 0.5 and 50 mg L(-1) , respectively. The LDH leakage and inhibition of albumin synthesis, along with decreased ALT activity, indicated that treatment with either AgNP or Ag ions resulted in membrane damage and reduced the cell function of human liver cells. Evaluation of oxidative stress markers demonstrating depletion of GSH, increased ROS production, and increased SOD activity, indicated that oxidative stress might contribute to the toxicity effects of nano and ionic forms of silver. The observed toxic effect of AgNP on HepG2 cells was substantially weaker than that caused by ionic silver, while the uptake of nano and ionic forms of silver by HepG2 cells was nearly the same. © 2014 Wiley Periodicals, Inc. Environ Toxicol 31: 679-692, 2016., (© 2014 Wiley Periodicals, Inc.)

In the pathogenesis of asthma, oxidative stress appears to play an important role and existence of an oxidant/antioxidant imbalance is evident. In this study the key markers of oxidative stress and lipid peroxidation in the pathogenesis of asthma in childhood in comparison to healthy subjects were investigated. Plasma marker of the lipid peroxidation: malondialdehyde (MDA), the erythrocytes antioxidative enzymes: glutathione peroxidase (GSH-Px), superoxide dismutase (SOD), glutathione reductase (GR) and cysteine-containing tripeptide glutathione (GSH) were evaluated by spectrophotometric methods using blood samples collected from 37 healthy children and 44 asthmatic patients. The GSH-Px activity was significantly lower in asthmatic children (3.99 +/- 1.0 IU/g Hb) than in healthy controls (4.61 +/- 1.3 IU/g Hb; p < 0.034). Significant difference in activity of the SOD, GR, and concentration of cysteine-containing tripeptide GSH was not confirmed (p > 0.05). Lower GSH-Px activity in children with controlled asthma showed deficient erythrocyte antioxidant defence and evidence of association between oxidative stress and asthma in childhood. Preserved activity of GR and SOD, together with concentration of GSH and MDA, still seems to be crucial in controlling antioxidant/oxidant balance of the disease.

Abstract: Pelargonium radula (Cav.) L''Hér is a plant with hypoglycaemic properties originating from South Africa. Since oxidative stress plays a major role in the development of diabetic complications, the aim of this study was to evaluate if P. radula, besides its glucose-lowering properties, can have additional beneficial effects on diabetes. For preparation of extracts fresh or dried leaves were extracted at 20°C with either ethanol or water. Since P. radula is commercially cultivated for its essential oil, the residues obtained after steam distillation of essential oil from dry or fresh leaves were also included in the investigation. Content of phenols (total phenols, flavonoids and tannins) was determined in the extracts. Antioxidant activity was established as radical scavenging and chelating activity, reducing power and activity in β-carotene-linoleic acid assay. To establish possible intracellular effects of the extracts, lactate dehydrogenase (LDH) leakage was determined in Hep G2 cells with glucose induced oxidative stress. All the extracts were found to possess antioxidant activities and were able to reduce LDH leakage from Hep G2 cells. In addition to having excellent extraction yields the residues obtained after steam distillation of essential oil showed the most pronounced antioxidant activity in our study. The results of the present study suggest that P. radula leaf might be useful as complementary therapy in diabetes. [Copyright &y& Elsevier]

Background: Oxidative stress is believed to play a pivotal role in the etiology and pathogenesis of diabetes mellitus and its late complications. Hyperglycaemia- induced oxidative stress in diabetes is a consequence of both increased production of free radicals and reduced capacity of antioxidative defence. The citrus-derived flavonoid, naringenin, possesses antioxidative, free radical scavenging and metal chelating properties. The aim of this work was to investigate the antioxidative effect of naringenin on the activities of superoxide dismutase (SOD) and glutathione peroxidase (GPx) in HepG2 cells under hyperglycaemic conditions. Materials and methods: Activities of SOD and GPx were measured in lysates of HepG2 cells (ATCC HB8065, Manassas, USA). HepG2 cells tested were divided in six groups: control group, diabetes group (30 mM glucose) and four diabetes-naringenin groups (30 mM glucose + naringenin in one of the following concentrations: 1000, 100, 10 and 1 μg/mL). Activities of both enzymes were measured spectrophotometrically and expressed by protein concentrations. Results: The results were reported as specific activities of SOD and GPx. All groups tested were compared to diabetes group. Student t-test was used to compare tested groups. P-value <0.05 was adopted as statistically significant. Diabetes-naringenin group (30 mM glucose + 1 μg/mL naringenin) showed significantly increased activities of SOD (P<0.001) and GPx (P=0.007). On the other hand, in diabetes-naringenin group (30mM glucose + 10 μg/mL naringenin) only SOD showed increased activity (P=0.002). The other two diabetesnaringenin groups did not show significantly higher activities of SOD and GPx. Conclusion: The results obtained from this work indicate that naringenin exhibits its antioxidative effect on the activity of SOD and GPx in HepG2 cells under hyperglycaemic conditions when applied in lower concentrations, 1 μg/mL and 10 μg/ mL. [ABSTRACT FROM AUTHOR]