Academic Thesis

Basic information

Name Ikeda Shiyogo
Belonging department
Occupation name
researchmap researcher code 1000113908
researchmap agency Okayama University of Science

Title

Suppressive Effects of Natural Compounds on Methionine Auxotrophy of a Cu,Zn-Superoxide Dismutase-Deficient Mutant of Saccharomyces cerevisiae

Bibliography Type

Author

Shogo Ikeda, Takanori Senoo, Shinji Kawano, Sayaka Tamura, Yuki Shinozuka, and Shihori Sugishita

Summary

Yeast lacking Cu,Zn-superoxide dismutase (sod1∆) exhibits methionine (Met) auxotrophy, primarily due to the depletion of NADPH required in the sulfur assimilation pathway by oxidative stress. In this study, we measured the ability of natural compounds, including ingredients in foods and dietary supplements, to restore the cell growth of sod1∆ in liquid and solid media without Met. Homocysteine at around 0.1 mM fully suppressed auxotrophy but in excess (> 0.4 mM) had a harmful effect. Methionine sulfoxide at concentrations from 0.05 to 0.8 mM and S-adenosylmethione (0.05 to 6.2 mM) completely relieved the growth defects caused by sod1∆. Ascorbic acid (1 to 50 mM) restored sod1∆ growth, indicating that the action of this antioxidant could improve Met biosynthesis. However, ascorbic acid derivatives, ascorbic acid 2-glucoside and dehydroascorbic acid, did not show any activity. The suppressive effects of cysteine, N-acetylcysteine, and glutathione peaked at 0.1 mM, 0.5 mM, and 0.05 mM, respectively, but an excess of these agents was less effective. Suppression by dithiothreitol confirms that the thiol group is responsible for the amelioration of Met biosynthesis. No growth was restored for other categories of antioxidants including polyphenols, Trolox, melatonin, astaxanthin, and others.


Magazine(name)

Food Science and Technology Research

Publisher

Volume

21

Number Of Pages

1

StartingPage

137

EndingPage

143

Date of Issue

2015/01

Referee

Exist

Invited

Not exist

Language

English

Thesis Type

Research papers (academic journals)

ISSN

DOI

NAID

PMID

URL

J-GLOBAL ID

arXiv ID

ORCID Put Code

DBLP ID