130. 2012年5月29日 03:02:41
: Mnxczxr6Dw
「英語を読めること」だけを自慢していたバカが、自称ケーザイ学者で本職は「煽りチンドン屋」の
池沼信夫がどっかから引っぱってきたアメリカのチンドン屋の記事を自慢げに
さらしていたけど、そういうバカをつぶす「毒消し」を貼っておきますよ～。（笑）
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The Institute of Science in Society
Science Society Sustainability
http://www.i-sis.org.uk
This article can be found on the I-SIS website at
http://www.i-sis.org.uk/Bystander_Effects_Multiply_Dose.php ========================================================
ISIS Report 28/05/12
Bystander Effects Multiply Dose & Harm from Ionizing Radiation
############################################################## Effects of radiation felt by non-radiated neighbouring cells prompt a rethink of
radiation risk, radiotherapy and radioprotection. Dr. Mae-Wan Ho Low dose big effects Linear dose response relationships are routinely used in risk assessments of
exposure to environmental hazards, and ionizing radiation is no exception.
Typically, effects at high doses that kill cells, cause gene mutations and
cancers, are back extrapolated to obtain an exposure limit at which the harm
caused is considered miniscule or acceptable in view of the benefits gained.
Ionizing radiation was widely believed to cause mutations by directly breaking
the bonds of DNA molecules in the nucleus. In the early 1990s, Hatsumi Nagasawa and John Little at Harvard School of Public
Health, Boston, Massachusetts, discovered, to their surprise, that while a
linear relationship applies to high doses of a-radiation (from 5cGy to 1.2 Gy,
where cGy = 10-2Gy) (see Box), a much enhanced effect was obtained at very low
doses of 0.03 cGy to 0. 25 cGy, when 30 to 45 % of the cells in a population of
Chinese hamster cells exhibited sister chromatid exchange (SCE involving double-
stranded DNA breaks). At that low dose of radiation, only 0.07 to 0.6 % of the
nuclei should have been directly hit by an alpha-particle. Yet the frequency of
SCE rose rapidly at very low doses reaching a plateau below 1 cGy, after which
no further increase occurred with increasing dose, though a decline occurred at
higher doses. That was the first indication that damaging signals may be
transmitted from irradiated to neighbouring non-irradiated cells in a
population, and they called it “the bystander effect” [1]. In another experiment they looked at mutation frequency of a specific enzyme,
and found the same enhanced effect at very low dose. At the lowest dose of 0.83
cGy, the efficiency with which the alpha-particle can induce a mutation
increases nearly five-fold; the mutation frequency was the same as that due a
dose 100 times as great (0.83 Gy). Using the then newly developed microbeam of very low dose alpha particles to
target individual cells, researchers at Columbia University, New York, showed
that hitting the cytoplasm was sufficient to induce mutation in the nucleus [3].
They commented that low dose radiation is all the more dangerous because it does
not kill the targeted cell, but allows its influence to spread widely to
adjacent cells, thus multiplying the radiation effect (about 100 fold). Absorbed dose, equivalent dose and effect dose Radioactivity is measured physically as Curies (1 Ci = 3.7 x1010 disintegrations
per second). But that does not take account of the energy of different kinds of
radiation and their interaction with biological tissues. The absorbed dose, Gray (Gy) is equal to and energy of 1 Joule/ kg absorbed. The equivalent dose Sievert (Si), is weighted by biological potency of different
kinds of radiation (1 for g-rays, b-particles, and X-rays, 20 for a-particles
and 10 for neutrons). The effective dose also in Sievert takes into account the
sensitivities of different tissues, applying weighting factors derived from
previous epidemiological studies of radio-induced cancers. Thus, lots of
judgements are used in arriving at the effective dose, based on a model of
linear energy transfer (and linear dose response relationship) that has proven
inapplicable for cells and organisms. Bystander effects now abundantly confirmed Since then, a wide range of bystander effects in cells not directly exposed to
ionizing radiation have been found, which are the same as or similar to those in
the cells that were exposed [4], including cell death and chromosomal
instability. Actually, radiation induced bystander effects have been described as far back as
1954, when factors that cause damage to chromosomes could be detected in the
blood of irradiated patients. Carmel Mothersill and Colin Seymour at McMaster
University published a key paper in 1997 showing that filtered medium from
irradiated human epithelial cells can reduce the survival of unirradiated cells,
suggesting that soluble factors produced by the irradiated cells were involved
in the bystander effects [5]. Indeed, serum from cancer patients treated with radiotherapy also causes cell
death and chromosomal instability in unexposed cells in culture, and this has
been shown as far back as 1968 [6]. In 2001, researchers at Columbia University, New York used microbeams to target
single cells with exactly defined numbers of a-particles. They found that
hitting 10 % of the cells induced the same frequency of cancerous transformation
as when every cell in the dish was targeted [7]. More recently, bystander DNA double-strand breaks were induced in a three-
dimensional human tissue culture that is closer to in vivo conditions. The
results obtained by the team led by Olga Sedelnikova at the National Cancer
Institute, Bethesda, Maryland, were much more dramatic. In marked contrast to
cultured cells in two-dimensions where maximal DSB occurred 30 minutes after
irradiation, the incidence of DSBs in bystander cells reached a maximum between
12 to 48 hours after irradiation, gradually decreasing only over 7 days. At the
maximum, 40 to 60 % of cells were affected [8]. These increases in bystander
DSBs were followed by increased apoptosis and micronucleus formation, loss of
nuclear DNA methylation and increased fractions of senescent cells. The authors
commented that treatment of primary tumours with radiation therapy frequently
results in the growth of a secondary malignancy of the same or different origin.
They raised the question on whether bystander effects could introduce negative
complications in radiation therapy, such as genomic instability in normal
tissues. They concluded that induced senescence might be a protective mechanism.
On the other hand, failure of these protective pathways can lead to the
appearance of proliferating, damaged cells and to an increased probability of
oncogenic transformation. New research from the University of Pittsburgh Pennsylvania throws further light
on the implications of bystander effects for radiotherapy. It is customary for
patients receiving bone-marrow transplant to undergo whole body irradiation to
kill the bone marrow cells of the host so as to encourage repopulation by
transplanted cells. The researcher found that irradiated mouse recipients
significantly impaired the long-term repopulating ability of transplanted mouse
haematopoietic stem cells (HSCs) 17 hours after exposure to irradiated hosts,
and before the cells began to divide. There was an increase in acute cell death
associated with accelerated proliferation of the bystander HSCs. The effect was
marked by a dramatic down-regulation of c-Kit (a proto-oncogene), apparently
because of elevated reactive oxygen species (ROS). Administration of an
antioxidant chemical or ectopically over-expression of a ROS scavenging enzyme
catalase improved the function of transplanted HSCs in the irradiated hosts [9].
This obviously has implications for protecting patients during radiotherapy as
well as those receiving bone-marrow transplant. Read the rest of this report on the ISIS website
http://www.i-sis.org.uk/Bystander_Effects_Multiply_Dose.php Or read other ISIS reports on science and energy
http://www.i-sis.org.uk/scienergy.php
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This article can be found on the I-SIS website at
http://www.i-sis.org.uk/Bystander_Effects_Multiply_Dose.php ━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
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