Lipid peroxidation in brain tissue following administration of low and high doses of arsenite and L-ascorbate in Wistar strain rats

Abstract

This study aimed at investigating the mechanism by which sodium arsenite induces brain injury and the role of L-ascorbate. Thirty adult (n=5) Wistar rats weighing between 140 and 160 g were used. Group 1 neither received sodium arsenite nor L-ascorbate (control), group 2 was administered low dose of arsenite only, group 3 received high dose of arsenite only, group 4 was administered L-ascorbate only, group 5 was administered low dose of arsenite and L-ascorbate, and group 6 received high dose of arsenite and L-ascorbate. M0 alon dialdehyde, MDA, levels were significantly increased in rats treated with high dose of arsenite when compared with those treated with low dose of arsenite. However, all treated groups except those treated with L-ascorbate only showed significant increase in MDA levels when compared with the control group. Rats treated with high dose of arsenite and L-ascorbate showed a significantly higher MDA level than those treated with low dose of arsenite and L-ascorbate. However, catalase activity, body weight gain, brain weight and mean food consumption were comparable across all groups. Brain tissue total protein was similar in all groups except in both groups treated with high dose of arsenite, where they were significantly reduced when compared with the control group. I0 n conclusion, sodium arsenite treatment induces brain injury via a mechanism associated with lipid peroxidation, but not catalase-dependent. However, L-ascorbate ameliorates arsenite-induced oxidative injury in the brain. L-ascorbate antioxidative potential in alleviating arsenite-induced brain injury is dependent on the concentration of arsenite.

A tRNA-derived RNA Fragment Plays an Important Role in the Mechanism of Arsenite -induced Cellular Responses

“…As discussed, arsenite is an important health risk factor and its contribution to respiratory illness is significant, with mechanisms largely unknown 45 . The investigated response to arsenite treatment is mainly oxidative stress and its regulation at the protein level 46 , 47 . It has been suggested that cells deficient in eIF2α phosphorylation have a higher accumulation of tRNA fragments derived from initiator-tRNA Met in response to arsenite, which may affect the rates of protein synthesis 16 .…”

In vivo exposure to codeine induces reproductive toxicity: role of HER2 and p53/Bcl-2 signaling pathway

“…Markers of oxidative stress were determined spectrophotometrically. Ferrous Oxidation-Xylenol Assay with Triphenylphosphine was employed to assess the production of hydrogen peroxide as previously described [ 5 , 32 ], while malondialdehyde (MDA) levels were identified as a product of lipid peroxidation by measuring thiobarbituric acid reactive substances (TBARS) [ 5 , 33 ]. The testicular concentrations of Advanced Glycation Endproducts (AGE), a product of oxidative protein denaturation, was determined by ELISA method using standard kits according to the manufacturer's guideline (Elabscience Biotechnology Co Ltd, USA), while reduced glutathione (GSH) levels were determined by spectrophotometric methods using Ellman's procedure [ 5 , 34 ].…”

Testicular toxicity following chronic codeine administration is via oxidative DNA damage and up-regulation of NO/TNF-α and caspase 3 activities

“…Lipid peroxidation concentration determination is by measuring the thiobarbituric acid reactive substances (TBARS) produced during lipid peroxidation as previously documented [30]. This method is dependent on the reaction between 2-thiobarbituric acid (TBA) and malondialdehyde, an end product of lipid peroxidation.…”