Effect of dietary antioxidants on the cytostatic effect of acrylamide during copper-deficiency in Saccharomyces cerevisiae

Abstract

Acrylamide exposure increases oxidative stress and causes cytotoxicity. In order to understand the role of oxidative stress in acrylamide toxicity, we utilized Saccharomyces cerevisiae as a model organism grown in Yeast Peptone Dextrose (YPD) or Copper-Deficient Medium (CDM). Although the growth curves of yeast were comparable in these media, acrylamide treatment resulted in significant growth inhibition and colony formation only in the CDM. Copper-deficiency induced a decrease in the intracellular metallothionein levels, along with reduced Cu, Zn-SOD activity that appeared to increase the sensitivity of the yeast to the cytostatic effect of acrylamide. Increased dichlorofluorescein (DCF) fluorescence, enhanced formation of para-phenyl tertiary butyl nitrone (PBN)-hydroxyethyl adducts and a lowered reduced glutathione (GSH) content were observed under copper-deficient conditions, when challenged with acrylamide. The cytostatic effects and intracellular redox changes in response to acrylamide were ameliorated by antioxidant molecules viz. a viz. curcumin, β-carotene, vanillin and caffeic acid, which effectively decreased the oxidative stress and improved the growth recovery.

Preventive Effects of Three Polysaccharides on the Oxidative Stress Induced by Acrylamide in a Saccharomyces cerevisiae Model

“…The inhibition of AA on yeast proliferation was mainly reflected in three aspects: firstly, it reduced the rate of yeast proliferation; secondly, the yeast inoculated in the medium containing AA had a longer lag phase; thirdly, the maximum density of yeast proliferation was significantly reduced. This result is consistent with the study on AA cytotoxicity using yeast as a model, but previous studies did not explore the effect of AA on the growth kinetics parameters of yeast [ 3 , 4 ].…”

“…This inconsistency may be attributed to the following three aspects: different experimental models, different doses of AA, and different observation time points. In this study, SOD activity in the cells exposed to AA for 2 h was lower than that in the vehicle group, and the results obtained by using a lower dose of AA (about 14 mM) in similar studies were that SOD was activated [ 3 ]. Therefore, under the intervention of high concentration of AA, SOD activity will be inhibited.…”

“…The observation result of some studies is that under the administration of AA, SOD enzyme activity was significantly inhibited, which indicates that AA induced redox imbalance and the antioxidant defense system failed to combat the influx of ROS [ 31 , 40 , 41 , 42 ]. In contrast, another part of the study showed that the stimulation of AA increased the activity of SOD, and it is thought to be a compensatory mechanism against oxidative stress [ 3 , 20 , 43 ]. This inconsistency may be attributed to the following three aspects: different experimental models, different doses of AA, and different observation time points.…”

“…In 1994, AA was classified as group 2A carcinogen by the International Agency for Research on Cancer [ 2 ]. Due to the Maillard reaction between asparagine residues and reducing sugars, heat-processed foodstuffs, such as potato products, bread, cereals and coffee, produce AA that is one of the main environmental sources of human exposure [ 3 , 4 ]. One of the important toxicological mechanisms is that AA mediates intracellular oxidative stress by promoting generation of reactive oxygen species (ROS), leading to the depletion of glutathione (GSH), and consequent DNA damage [ 5 , 6 ].…”

The Effect of Berry Juices on the Level of Oxidative Stress in Yeast Cells Exposed to Acrylamide

“…; Kommuguri et al . ). Additionally, we have shown that the berry juices significantly protect both WT and Δ sod1 cells against an inhibition of growth caused by acrylamide.…”