The present study investigated the effect of long-term intake of aspartame, a widely used artificial sweetener, on antioxidant defense status in the rat brain. Male Wistar rats weighing 150-175 g were randomly divided into three groups as follows: The first group was given aspartame at a dose of 500 mg/kg body weight (b.w.); the second group was given aspartame at dose of 1,000 mg/kg b.w., respectively, in a total volume of 3 mL of water; and the control rats received 3 mL of distilled water. Oral intubations were done in the morning, daily for 180 days. The concentration of reduced glutathione (GSH) and the activity of glutathione reductase (GR) were significantly reduced in the brain of rats that had received the dose of 1,000 mg/kg b.w. of aspartame, whereas only a significant reduction in GSH concentration was observed in the 500-mg/kg b.w. aspartame-treated group. Histopathological examination revealed mild vascular congestion in the 1,000 mg/kg b.w. group of aspartame-treated rats. The results of this experiment indicate that long-term consumption of aspartame leads to an imbalance in the antioxidant/pro-oxidant status in the brain, mainly through the mechanism involving the glutathione-dependent system.
In this article, pure and 2 M% dysprosium (Dy)-doped α-MoO3 nanobelts have been successfully synthesised by the autoclave assisted-hydrothermal method. The x-ray diffraction (XRD) patterns revealed that the nanobelts were crystalline in nature with an orthorhombic structure. The sharp and narrow XRD peaks divulged the high quality with good crystallinity of the nanobelts. The intensity of the peak (040) increased and shifted towards lower 2θ values which reflected the successful incorporation of Dy in MoO3 matrix. The scanning electron microscopy (SEM) images revealed the formation of randomly distributed nanobelts with average width of 90–150 nm and length of 950–1300 nm. Vibration behaviour of chemical bonds was characterised by Fourier-transform infrared spectroscopy (FTIR) and the detected peaks confirm the formation of orthorhombic structure of MoO3. The energy dispersive x-ray spectroscopy (EDX) spectra confirmed the Dy incorporation in the MoO3 matrix. Debye–Scherrer method, Wilson method, Williamson Hall (W − H) and Halder-Wagner (H − W) analyses have been employed to investigate the different parameters (such as crystallite size and lattice strain) and to analyse their contribution on the XRD peak broadening of the nanobelts. The crystallinity improved as the average crystallite size increased, and FWHM, lattice strain and dislocation density decreased after Dy doping. The obtained values of crystallite size estimated using Debye–Scherrer equation, and W − H and H − W plots, are nearly similar, highly inter-correlated and in the range of 26.06–31.44 nm. The Halder-Wagner (H-W) plots give the more precise results of different microstructural parameters by analysing XRD peak broadening of both samples compared to Debye–Scherrer and Williamson Hall methods.
Arsenic trioxide (AsO) is a highly effective therapeutic against acute promyelocytic leukaemia, but its clinical efficacy is burdened by serious cardiac toxicity. The present study was performed to evaluate the effect of omega (ω)-3 fatty acid on AsO-induced cardiac toxicity in in vivo and in vitro settings. In in vivo experiments, male Wistar rats were orally administered with AsO 4 mg/kg body weight for a period of 45 days and cardiotoxicity was assessed. AsO significantly increased the tissue arsenic deposition, micronuclei frequency and creatine kinase (CK)-MB activity. There were a rise in lipid peroxidation and a decline in reduced glutathione, glutathione peroxidase, glutathione-S-transferase, superoxide dismutase and catalase in heart tissue of arsenic-administered rats. The cardioprotective role of ω-3 fatty acid was assessed by combination treatment with AsO. ω-3 fatty acid co-administration with AsO significantly alleviated these changes. In in vitro study using H9c2 cardiomyocytes, AsO treatment induced alterations in cell viability, lactate dehydrogenase (LDH) release, lipid peroxidation, cellular calcium levels and mitochondrial membrane potential (∆Ψ). ω-3 fatty acid co-treatment significantly increased cardiomyocyte viability, reduced LDH release, lipid peroxidation and intracellular calcium concentration and improved the ∆Ψ. These findings suggested that the ω-3 fatty acid has the potential to protect against AsO-induced cardiotoxicity.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.