j
I
n ot explain this paradoxical effect, but
w‘e should mention that Bloom et al.
aIso failed to detect a relation between
chromosomally abnormal survivors in
1Iiroshima and Nagasaki and their estinmted doses of radiation (8). Chromos’ome aberrations did not correlate with
a,ge or sex, nor could any relation
t~e established between the occurrence
c~f thyroid lesions and chromosome ab1normalities.
We cannot account for the unusualIy
]igh incidence of acentric fragments in
he unexposed and their relative deficit
n the exposed people. Radiation from
ngested radionuclides is not likely to
be a factor, since all Marshall Islanders have been exposed to low levels of
I residual radionuclides, such as Cs1g7,
Znos, and Sr~O since their return to
Rongelap in 1957, and since body bur-.
dens of these elements were about the
I
same in both groups. Although viruses
i and some chemicals, in addition to
ionizing radiations, are known to produce breaks in human chromosomes in
1 vivo and in vitro (13), the kind and
distribution of the fragments seen in the
cells of the unexposed group do not
suggest this origin. If these agents were
implicated, it is not clear why they
faiIed to produce a similar effect in
the exposed people who have lived on
the same island under identical environmental conditions since 1957.
Similar chromosome aberrations have
been reported in the Japanese fishermen
exposed to radiation from the same
fallout (7); the incidence of abexations,
excluding aneuploid cells, was 2.1 perI
cent and thus identical with our finding:
most were two-b~eak aberrations. The
incidence of acentric fragments in a
control population of Japanese studied
I by the same authors was 0.11 percent
—20 times less than our finding among
tire eight unexposed Marshall Islanders.
In ‘a controlled cytogenetic study of
sampled survivors of the atomic bombings of Hiroshima
and Nagasaki,
Bloom et al. have found exchange-type
chromosome aberrations in 33 persons
—3s percent of 94 survivors examined
20 years after exposure (8); the incidence of aberrations
was 0.6 peri
cent in the exposed group-less
than
half our finding among the Marshall
I Islanders. Bloom et al. found only a
single acentric fragment in 8847 cells
from the 94 controls, an incidence of
0.01 percent; for the 33 aberration-positive individuals, the dose ranged from
237 to 891 rads, and for none of the
I
I
I
I
1
I
1
I
I
1.
I
I
Ii
I
2S JULY 1967
entire group was it less than 200 rads.
All persons examined were 30 years
of age or younger at the time of the
bombings.
The results of our study demonstrate
that a small but significant number of
chromosome
aberrations
persists
in
blood lymphocytes of some Marshall
[slanders 10 years after exposure to
fallout radiation. The conclusion that
at least some of these aberrations were
caused by the radiation, and not by
other factors, rests on the finding that
exchange-type aberrations were found
only in the exposed people and not
among the controls.
The biologic significance of persistent
chromosome aberrations in blood lymphocytes
of hematologically
normal
persons many years after exposure to
ionizing radiation is not known.’ In
particular, any role that aberrations of
this type may play in the pathogenesis
of radiation-induced
leukemia can only
be surmised at present. It is problematical and indeed doubtful whether chromosome aberrations in lymphocytes can
serve to indicate abnormalities in other
tissues, except perhaps inferentially. Indeed, of the ten individuals who have
developed thyroid lesions since our examinations were made, only three show
double-break aberrations.
HERMANN
Lrsco
E. Nasjleti acsd H. H. Spencer, Cancer
Re$. 26, 2437 (1966); W. W. Nichols, Amer.
J. Human Genet. 1S, 81 (1966).
14. Stmmrted
by AEC (Brookbaven National
La-b-oratory), - the Trtr& Territory of the
tkit’ic
Islands, AEC contrsct AT(30-1)-3777
with New En@nd Deaconesa Hospital, and
PHS grant CA-06930. Fur expert assistance
we thank V. Eswy, L Irwin, and W. Merrill
of New Enslmd Deaconess Hospital, Boston
(with the chromosome snalysis); smd P.
Crumrine, R. Hsmmerstro~
W. A. Scott,
rind W. Waithe of Bruokhaven National
Laboratory. We shank S. M. Shea for help
with the statistics, and msny individusts in
AEC and the Tmst Territory of the Pacific
Islsnds for their support.
13. C.
8 ?&y
1967
Chhmydomonas
Heterozygous
reinhtsrdi:
Diploid
Sttains
“”
Abstract. Zygotes of the unicelhdar
reinhardi
green alga Chlamydomonas
occasionally
divide mitotica[ly
tw give
rise to stable diploid vegetative strains.
As well as by ~heir mode of origin;
these strains
are distinguished
front
hap[oids by cell and nuclear size, DNA
content per nucleus, and chromosome
number.
Diploid
strains heterozygous
for a variety of mutant genes are phewild type and mating-type
notypicaliy
minus.
Thus these mutant genes are
recessive to their wild-type alleies, and
the mating-type-minus
is dominant over
the mating-type-plus
allele.
Cancer Research Institute, New England
of
Deaconess Hospital, and Department
Pathology, Haward Medical School,
Boston, Massachusetts
02215
The life cycle of the unicellular green
reinhardi, as typialga Chlamydomonas
cally described, involves the fusion of
two haploid gametes to form a diploid
ROBERT A. CONARD
zygote which then develops into a thickMedical Department,
Brookha,ven
walled resting . cell (mature zygote).
National Laboratory
Upton,
Mature zygotes undergo meiosis and
Long Island, New York 11973
germinate
to produce four or eight
haploid
cells
that are capable of vegetaRefarances and Notes
tive growth.
L L M. Toush, K. 33. Buckron. A. G. Baikie.
W. M. Court-Brown, Larccet 1960-3S, S49
Recently it has been observed that
(19cWX K. E. Buckton, P. A. Jacobs. W. M.
newly formed zygotes may follow an
Court-Brown. R. A. Doll, ibid. 1962.11, 676
(1%2).
alternate
course of development
(IY
2 S. Warren and L. Meiacrer, J. Amer. Med.
AJsor. 193, 3St (196S); R. E. Millard. Cyro-.
rather than differentiating into mature
genetics 4. 277 ( 1%5): P. C. NowelI. Mood
zygotes, some may divide mitotically to
26, 798 (1%5): hi. Bacschingcr and 0. HUL
Srmhlenrhcrscpic 131, t09(1966).
give rise to diploid cells that remain
3. A, D. Bluom and J. H. Tjio, New Errg. J.
vegetative. I now describe a selective
Med. 270, 1341 (1964).
4. A. Normsn. M. Sasaki, R. E. Ottoman. R. C.
method -for obtaining diploid strains,
Veomett. Radiation Res. 23, 282 (1964).
5. M. A. Bender and P. C. Gouch. ibid. 18,
and some of the characteristics that dk389 (1%3):
ibid. 29, 56S ( 1966).
tinguish
them from haploid strains.
6. ~i Dgi&%;
SuSahar& M. Horikawa, fbfd.
AMy method for recovering dlploid
7. T.’ Ishihara aid T. Kumatori, Ac:a Hacmatol.
strains is based upon the inability of
Jwmr. 2S. 291 (196S).
S. A. D. Bluom, S. Neriishi, N. Kacnada. T.
mutant
auxotrophic
haploid cells to
Iseki, R. J. Keehn, I.uncrr 1966-11,672 (1966).
9. R. A. Conard and A. Hick in~, ./. Amer. Med.
grow under conditions that allow protoASSOC. 192; 457 [ 1965).
10. R. A. Conard. J. E; l{all, W. W. SUIOW, trophic CCIISto proliferate rapidly. These
Ncw Ihf. J. Med. 274. 1?91 (1966).
conditions arc met by plating a mating
t]. P. S. Moorhead, P. C. Newell, W. J. MeIl.
mixture of two different auxotrophs on
man. D. M. Battipx, D. A. Hungerfm.1,
EXp. Cd Res. 20, 613 ( 1960).
a minimal agar medium lacking the re12. K. E. Buckton and M. C. Pike, lrsierst. 3.
quired growth factors.
Rodintlon Biol. S, 439 (19h4).
447