Inhibition of acrolein-induced apoptosis by the antioxidant selenium

Abstract

In this study, the effects of a potent antioxidant, selenium, on apoptosis induced by acrolein, a cytotoxic and genotoxic environmental pollutant, were investigated by immunohistochemical and electron microscopic methods. One hundred adult male Wistar albino rats were used in the study. The rats were divided into four main groups: control, acrolein, selenium, and acrolein + selenium. The animals in the experimental groups were given 1 mg/kg/day selenium and 4 mg/kg/day acrolein daily for 7 days by gavage. After drug administration, each group was divided into subgroups according to the time they were to be euthanized: 12th hour, 1st, 2nd, 3rd, and 5th day. The rats in each group at the determined time were euthanized and their livers were removed. Routine histological procedures were performed for light and electron microscopy examinations. After applying the Terminal Deoxynucleotidyl Transferase dUTP nick end labeling assay on the liver sections, apoptotic index values were calculated. Comparing the liver sections of the rats in the acrolein group and the control group, acrolein was found to cause a significant increase in the apoptotic index. The apoptotic index values of the acrolein + selenium group decreased compared to the acrolein group. In the electron microscopic examinations, apoptotic findings were observed in the liver tissues of the rats given acrolein, such as chromatin condensation in the nucleus of hepatocytes, dilatations in the perinuclear space, and cytoplasmic vacuolization. These apoptotic findings were not observed in the acrolein + selenium group after the 12th hour. These findings show that selenium may potentially be useful as a protective agent for people exposed to acrolein.

Molecular Mechanisms of Selenium Mitigating Lead Toxicity in Chickens via Mitochondrial Pathway: Selenoproteins, Oxidative Stress, HSPs, and Apoptosis

“…Se supplementation ameliorated cerebral injury caused by mercury and Pb in chickens [ 8 , 34 ]. An investigation recorded that Se alleviated apoptotic damage caused by the environmental pollutant acrolein in rat livers [ 35 ]. Similar to the above findings, we also found that Se supplementation relived Pb-induced apoptotic damage in both chicken cerebellums and thalami.…”

Potential adverse health effects of dietary lipid oxidation products

“…Kang and co-authors found that oral daily exposure to HNE (0.5 mg/kg) for 28 days produced hepatotoxicity in rats, as evidenced by significant alterations in serum albumin, serum total bilirubin, and aspartate aminotransferase (AST) activity (Kang et al, 2011). In addition to HNE, Gökçe et al (2020) reported that consumption of acrolein (4 mg/kg) for 7 days by gavage induced liver tissues apoptosis in rats, as evidenced by chromatin condensation in the nucleus of hepatocytes, dilatations in the perinuclear space, and cytoplasmic vacuolization.…”

The role of endoplasmic reticulum stress in lead (Pb)-induced mitophagy of HEK293 cells

“…More recent studies have unveiled that some of the toxic effects of Pb are also localized to the endoplasmic reticulum (ER), which controls a wide range of cellular processes (Corsetti et al, 2017; Jia et al, 2018). A variety of stimuli such as calcium deprivation, oxidative stress, and exogenous toxins would initiate ER stress via a coordinated stress response called the unfolded protein response (UPR) (Gökçe et al, 2020). It has been found that UPR is restricted by three transmembrane ER stress sensors in mammalian cells, namely protein kinase R-like ER kinase (PERK), inositol-requiring protein-1α (IRE1α), and activating transcription factor 6 (ATF6) (Walter and Ron, 2011).…”