Public Health, Molecular and Cellular Biology

Environmental Medicine and Molecular Toxicology

Exploring of Physiologically Oriented Reactive Oxygen Species in Life Science and Molecular Toxicology

  • Master / Doctoral Degree


AKAIKE, TakaakiAKAIKE, Takaaki
AKAIKE, Takaaki

Professor, M.D. Ph.D.

Research Theme

  • Chemical biology of nitric oxide and reactive oxygen species and regulation of oxidative stress
  • Pathogenesis and epidemiology of emerging pathogen Helicobacter cinaedi
Research Keywords:

reactive oxygen species, oxidative stress, reactive sulfur species, metabolic syndrome, molecular toxicology

Technical Keywords:

chemical biology, proteome, metabolome

Laboratory Introduction

Reactive oxygen species (ROS) produced in excess in cells induces oxidative stress and is involved in various diseases including infection and inflammation, cancer, metabolic syndrome such as atherosclerosis and diabetes, and neurodegenerative disorders like Alzheimer's disease. In recent years, ROS are recognized as signaling molecules regulating various biological phenomena. ROS exerts various physiological functions such as adaptive response to oxidative stress, autophagy induction, and regulation of cell senescence and cell death, via well-organized signaling pathways consisted with receptor molecules and effector proteins. To clarify the regulation mechanism of ROS signaling is a high-priority subject in research on the pathogenesis of oxidative stress-related diseases.
Our laboratory investigates the molecular mechanism of infectious diseases as an environmental factor, toxicology of environmental pollutants, and cellular responses to environmental and oxidative stress, by using the advanced analytical techniques, such as chemical biology, proteomes, metabolomes, etc. Recent progresses in our study include the discoveries of the reactive sulfur species as new regulator of oxidative stress and the promotion of atherosclerosis by the infection of emerging pathogen Helicobacter cinaedi.
Based on these high-impact achievements, we are seeking to develop novel strategies of diagnosis, remedy, and prevention for various diseases, in view of the defense mechanism in response to oxidative stress.

Figure 1. Regulation of oxidative stress by reactive sulfur species

Figure 1. Regulation of oxidative stress by reactive sulfur species

Figure 2. Promotion of atherosclerosis by <i>Helicobacter cinaedi</i> infection

Figure 2. Promotion of atherosclerosis by <i>Helicobacter cinaedi</i> infection

Recent Publications

  • Ida T, et al. Reactive cysteine persulfides and S-polythiolation regulate oxidative stress and redox signaling. Proc Natl Acad Sci USA. 111(21):7606-7611, 2014
  • Khan S, et al. Promotion of atherosclerosis by Helicobacter cinaedi infection that involves macrophage-driven proinflammatory responses. Sci Rep. 4:4680, 2014
  • Yoshizawa T, et al. SIRT7 controls hepatic lipid metabolism by regulating the ubiquitin-proteasome pathway. Cell Metab. 19(4):712-721, 2014
  • Ito C, et al. Endogenous nitrated nucleotide is a key mediator of autophagy and innate defense against bacteria. Mol Cell. 52(6):794-804, 2013
  • Nishida M, et al. Hydrogen sulfide anion regulates redox signaling via electrophile sulfhydration. Nature Chem Biol. 8(8):714-724, 2012