Tocotrienol-Rich Fraction Modulates Genes Expression in Oxidative Stress-induced Caenorhabditis e legans

Abstract

Objective: The study was done to determine the effect of Tocotrienol rich fraction (TRF) on the expression of RNAs in C. elegans under oxidative stress.
 Methods: The nematodes were divided into 4 groups and treated accordingly: control; TRF; hydrogen peroxide (H202); TRF treatment before and after H202-induction (TRF+H202+TRF). Expressions of RNAs were analyzed with Affymetrix Genechip C. elegans Genome Array and Genespring GX11 software where differentially expressed genes were further analyzed using gene ontology (GO). Selected genes (unc-15, cit-1.2, ftn-1, rsks-1, unc-4 and daf-12) were analyzed with RT-qPCR to validate the results.
 Results: TRF modulated the expression of 314 genes involved in determination of adult lifespan, regulation of growth and lipid modification. A total of 440 genes involved in RNA metabolic processes, transcription, growth and differentiation of muscle and nerve cells were differently expressed following H202 induction. TRF treatment before and after H202- induction resulted in 438 differentially expressed genes involved in RNA metabolic processes, transcription, response to xenobiotic stimulus and protein amino acid phosphorylation.
 Conclusion: TRF modulates the expression of genes involved in the regulation of lifespan in C. elegans.
 Bangladesh Journal of Medical Science Vol.18(4) 2019 p.711-721

The Effect of Tocotrienol-Rich Fraction on the Expression of Glutathione S-Transferase Isoenzymes in Mice Liver

“…Out of all the genes affected, TRF administration significantly elevated the mRNA level of GST homologue in MDA-MB-231 but not in MCF-7 cells (Nesaretnam et al 2004). In Oxidative Stress-Induced Caenorhabditis elegans worms, TRF had been found to induce the expression of GSTP1 protein (Aan et al 2015). In another in vitro study involving human retinal pigment epithelial cells, pretreatment with α-tocopherol inhibited ROS generation, increased Nrf2 expression and induced many phase II enzymes such as GST (Feng et al 2010).…”

Paraoxonase-1 Enzyme Activity and Oxidative Status in Pulmonary Hypertension Original Article

“…Oxidative Stress (OS) has been considered to be one of pathophysilogical causes of molecular damage to cellular and tissue structures and implicated in the development of PH via leading to alteration of pulmonary vasomotor tone induced by hypoxia. [3][4][5] OS is an imbalance due to increased reactive oxygen or nitrogen species (ROS or RNS) with or without decreaesed antioxidant defense, can lead to cell damage by inhibition of protein, lipid, and DNA physiologic functions [3][4][5]11,12 . So, oxidative damage occurs when the production of ROS exceeds the scavenger capacity of the anti-oxidant mechanisms of the cell.…”