Worm Breeder's Gazette 13(5): 84 (February 1, 1995)

These abstracts should not be cited in bibliographies. Material contained herein should be treated as personal communication and should be cited as such only with the consent of the author.

mev-1 Is a Mutant of Premature Aging.

Hiroshi Adachi1,2, Hideaki Hosokawa2, Naoaki Ishii2

1 Research and Development Headquarters, Biological Science Research Center, Lion Corporation, Tajima, Odawara, Kanagawa, 100
2 Department of Molecular Biology, Tokai University School of Medicine, Isehara, Kanagawa 259-1 1, Japan

Mutation in mev-1 render animals hypersensitive to high
oxygen concentration (1). The life span of this mutant
is shorter than that of wild type under atmospheric conditions
and various depending upon the oxygen concentration (2).
To further our understanding of mev-1, we. measured the
level of peroxylipid and oxidized protein as assessed
by fluorescent materials and carbonyl residues, respectively.These
are good markers of aging, as it accumulated with increasing
aging.
Fluorescent materials in methanol/water extracts of
both wild type and mev -1 animals accumulated with increasing
age. The fluorescent material in mev-1 accumulated more
than in the wild type. The amount of the extracts of mev-1
on day 10 was approximately two times that observed in the
wild type on the same day (3). We also found that the mev-1
mutant accumuiates more carbonyl residues at a greater
rate than dose wild type.
When incubated under 90percent oxygen, the fluorescent
materials in the mev-1, but not wild-type animals accumulated
more rapidly compared with when incubated under atmospheric
condition. Conversely, the materials did not accumulated
in either wild type or mev-1 animals under 2percent oxygen3.
The rate of accumulation of fluorescent material was influenced
by oxygen.The activity of superoxide dismutase was about
half the wild-type level(1). These observation suggests
that the mev-1 may be a mutant of premature aging and oxygen
may be a determinant of aging in C. elegans.
1. N. Ishii et al, Mutation Research, 237, 16*171
2. S. Honda et al, J. Geront.48, B*7-B61 (1993)
3. H. Hosokawa et al, Mech. Ageing Develop. 74, 161- 1 70
(1994)