Radiation Protection Dosimetry (2019), pp. 1–6 doi:10.

1093/rpd/ncy271

BIOPHOTONS IN RADIOBIOLOGY: INHIBITORS,

COMMUNICATORS AND REACTORS

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Carmel Mothersill1,*, Michelle Le1, Andrej Rusin1 and Colin Seymour2
1
Department of Biology, McMaster University, 1280 Main Street West, Hamilton, ON L83 4K1, Canada
2
Medical Physics, McMaster University, 1280 Main Street West, Hamilton, ON L83 4K1, Canada

*Corresponding author: mothers@mcmaster.ca

Radiation-induced bystander effects refer to the production of signals from irradiated cells which induce responses in unirra-
diated, or bystander, cells. There has been a recent resurgence of interest in low-energy photon biology. This is due to con-
cerns about health effects, increased use of biophoton imaging techniques, and the fact that biophotons can act as a bystander
signal. This review discusses the history of light signaling in biology and potential mechanisms involved in the generation and
transduction of signaling mechanisms. The role of photons in signaling in the animal and plant kingdoms is also reviewed.
Finally, the potential to harness these mechanisms in radiation protection or therapy is discussed with emphasis on promising
future directions for research.

BIOPHOTON PRODUCTION IN LIVING

SYSTEMS – HISTORICAL REVIEW
The phenomenon of spontaneous ultra-weak photon
emission (UPE) by biological systems was first docu-
mented in the 1930s where the photons from bio-
logical materials were measured using Geiger–Mueller
counters fit with quartz windows(1, 2). These pioneer
experiments revealed that the photon fluences emitted
from biological materials were relatively low, ranging
from 101 to 103 photons cm2 s−1(1, 2), the emitted
photons were either UV or contained a UV compo-
nent(3), and the photon emissions could be detected
from a variety of biological materials including
blood(4), bacteria(5) and tumor tissue(6). These photon
emissions were distinguished from luciferin- luciferase-
attributed bioluminescence since the photon yields in
this system were 103–106 times weaker than the levels
characteristic of luciferin–luciferase luminescence(7).
During the 1930s, the reports of positive photon emis-
sion were also challenged by negative results observed
by other researchers(8, 9). In the 1930s, the detection
systems were all developed and constructed manually,
thus it is likely that the detectors in each research
group possessed different sensitivity and possibly
explains the variability among the results observed(10).
Nevertheless, presence of evidence disproving the phe-
nomenon led to a diminishing interest in the effect
and scientific investigation into photon emission from
biological materials was not revived until the 1950s
when photomultiplier tubes (PMTs) became widely
available for measuring photon sources with relatively
low fluence(11, 12). Only following the application of
PMTs did detection of biological emissions become
more reliable and reproducible(10). Further character-
ization of these photon emissions demonstrated a
qualitative dependence upon biophoton signal strength
that did not adhere to the laws of linear physics.
VanWijk et al. demonstrated significantly greater pho-
ton emission from tumor cells than normal cells even
when each type of cell was maintained at the same
quantity(13). Such results suggested that photon emis-
sion was linked to biological processes and could not
be explained purely based upon physical expectations.
The phenomenon of biological photon emission was
given a name in 1984 when the German biophysicist
Dr Fritz-Albert Popp coined the term biophotons to
refer to the weak fluence of UV and visible range
photons emitted from biological systems(14). Up until
then, this phenomenon was often referred to as
UPE(10), although the name did not indicate specificity
to the photons’ biological origin. Presently, the two
terms are used interchangeably in the field of biopho-
tonic research.
Following the confirmed existence of biophotons,
the question of how the photons were being produced
and whether they had any downstream biological
effects arose as the two predominant lines of inquiry.
Based upon the available literature, the leading candi-
date for intracellular biophoton production is the
generation of excited species and their subsequent
relaxation to a stable state. Lipid peroxidation and
oxidative metabolism in the mitochondria can both
lead to the production of electronically-excited states
in biological systems(15). Both singlet oxygen (1O2)
and carbonyl compounds in the triplet state have been
identified as sources of biophoton emission by the
measurement of spectral emission following the use of
various excited species scavengers (i.e. β-carotene) and
sensitizers (i.e. rotenone)(16). Mitochondria are con-
sidered as a key source of biophoton emission because
of the abundance of molecular oxygen (ground state
triplet oxygen, 3O2) present in the mitochondrial
respiratory chain. The oxygen involved in the respira-
tory chain therefore predisposes the mitochondria to

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 C. MOTHERSILL ET AL.
an increased probability for 1O2 generation. Excitation
and subsequent change in electron spin of one of the
electrons in 3O2 results in the production of 1O2(17).
Because the probability for excitation of 3O2 is asso-
ciated with oxidant activity in the mitochondria, a rela-
tionship therefore exists between photon emission and
mitochondrial metabolic activity(17).
Nakano and colleagues provided evidence to sug-
gest that excited tryptophan and excited tyrosine,
produced as a result of oxidation by peroxidase, are
candidate sources of biophoton emission. Their
research supports these amino acids as potential bio-
photon sources since the emissions they observed
from sea urchin eggs undergoing fertilization (a pro-
cess associated with lipid peroxidation) coincided
very closely with the reference emission spectra of
excited tyrosine (478–500 nm) and excited trypto-
phan (550–610 nm)(18). The contribution of trypto-
phan, tyrosine, singlet oxygen and excited triplet
carbonyls collectively demonstrate the ability of cells
to emit biophotons ranging from UV all the way to
infrared (IR) wavelengths(19). While it is apparent
that the spectral distribution of biophoton emission
spans the UV, visible and IR regions, specific details
pertaining to the signal strength and fluence rate at
each wavelength still remain difficult to determine.
In the 1980s, Fritz-Albert Popp suggested that
DNA should be an important factor in the consider-
ation of a potential source of biophotons(14). His work
demonstrated evidence for the involvement of DNA
conformation in mediating biophoton emission.
BIOPHOTON-MEDIATED INTERCELLULAR
COMMUNICATION
Several papers suggest biological systems communi-
cate with each other via the exchange of biophoton
signals(6, 20–24). The first documented evidence of
intercellular communication via optical signaling
was reported by Dr Alexander Gurwitsch in 1923.
Gurwitsch reported the ability of an onion root
meristem to induce a 20–25% increase in the mitosis
rate of a neighboring onion root meristem placed
2 mm away for a 2-h duration(6). He noted that the
surface of the recipient onion root that was exposed
to the sender onion root exhibited a greater number
of dividing cells than did the opposite surface.
Further investigation led to the suggestion that the
responsible factor was light in the UV range since
the insertion of a glass plate 0.3 mm thick resulted in
the elimination of the effect while insertion of a thin-
ner (tens of μm) glass plate did not(25). Gurwitsch
called this observed phenomenon the mitogenetic
radiation theory after the observation that light
could stimulate mitosis(6). It was later confirmed that
UV light is indeed emitted from living cells upon
detection with sensitive photon counters (PMTs)(26, 27).
2
The involvement of UV biophotons in eliciting
optical intercellular communication has been further
supported by subsequent studies. Wainwright and col-
leagues demonstrated the induction of visible light
emission by bacteria separated from fungus by a layer
of quartz glass(28). However, upon separation of the
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bacteria from the fungus by UV-impermeable glass,
the effect was no longer observable(28). Belouuov and
Baskakov also reported a marked induction of acceler-
ated frog egg division (cleavage) upon exposure of
bystander eggs to the biophotons emitted from a dense
cluster of cleaving eggs; the two egg populations were
separated by quartz glass(29). Shen et al. have also
shown that biophotons are capable of triggering stress
responses in optically-coupled cell populations(20).
Since it has become apparent that not all biophoton-
mediated intercellular interactions result in proliferative
endpoints, it is suggested that it may be more suitable
to refer to these effects collectively as biophoton-
mediated communication effects as opposed to mitoge-
netic effects.
Further research has demonstrated a role for bio-
photonic exchange of information by wavelengths
extraneous to UV in inducing effects in biological
detectors, suggesting that the signal was not chem-
ical in nature but electromagnetic(21).
The idea that multiple biophotonic frequencies may
be employed in the endeavor to communicate cellular
information is one that has been proposed widely in
an effort to explain the ability of such low fluence sig-
nals to induce significant and observable biological
modifications(14, 30–32). Popp was the first to propose
the coherence of light as a means of communication
and information transfer within biological systems(14).
The concept of coherence describes the cooperative
action of multiple subunits in a given system to carry
out a function(32). Following this framework, Bajpai
proposed the role of quantum coherence in the ability
of biological systems to communicate with each other
via biophotons and subsequently regulate biological
processes(32). While extensive discussion on the topic
of quantum biology is beyond the scope of this
review, a brief explanation of the observed effects that
are difficult to rationalize using classical mechanisms
prescribes to the quantum coherence of light follow-
ing absorption by a recipient cell, and the use of that
coherence to maximize the efficiency of a given bio-
logical process by enacting simultaneous pathways in
an effort to achieve the desired outcome or effect(33).
A hypothesis such as that proposed by Bajpai is con-
ceivable based upon the elucidation of a role for
quantum coherence in explaining the efficiency of
photosynthesis(34). Another proposed mechanism of
cellular communication via biophotons is the encod-
ing of information in photon bursts resembling
binary-encoded data. Mayburov characterized photon
emission from fish and frog eggs using a PMT sensi-
tive to both UV and visible light to find that the
 BIOPHOTONS IN RADIOBIOLOGY: INHIBITORS, COMMUNICATORS AND REACTORS
photon emission signal integrated over all of the
wavelengths exhibited fluctuations in strength over
time(35). The time-dependent spectrum over 400 s
revealed distinct bursts of light at randomly inter-
spaced intervals and subsequent analysis of reporter
egg populations revealed an ability of the biophotons
to synchronize growth among those bystander eggs(35).
While typical biophoton fluence rates are relatively
low, the proposed mechanisms for communication pro-
vide a means of ascertaining how they may be capable
of eliciting effective signaling between biosystems.
The research on biophoton communication pre-
sented thus far has focused primarily upon effects
that result following exposure of bystander systems
to spontaneous, or unperturbed, sources of biopho-
tons. However, biophoton emission leading to inter-
cellular communication of effects can also be
induced by various stressors. Kaznacheev reported
distant intercellular electromagnetic interaction
between optically-coupled healthy human fibroblast
cells and human fibroblasts which were infected with
the Coxsackie A-13 virus or injured with mercuric
chloride(23). Interestingly, the unperturbed bystander
fibroblasts exhibited mitotic inhibition, nuclear con-
densation and subsequent cellular fragmentation;
effects that are all characteristic of a cellular
response to the Coxsackie A-13 virus. Further inves-
tigation was unable to isolate any viruses from the
bystander cultures(23), eliminating the possibility that
the virus could have traveled from the infected popu-
lation to the bystander population via chemical
means such as transfer of volatile molecules. It was
noted that the effects mimicked by the bystander
cells manifested following a 12–14 h temporal delay.
Reproduction of the same experiment using mercuric
chloride revealed the induction of granular and
vacuolar degeneration in the bystander cells follow-
ing receipt of biophotons signals through quartz
glass(23). These cellular symptoms again reflected the
manifestations characteristic of direct cytotoxicity by
mercuric chloride. A collective analysis of these
results leads to the inference that the effects directly
induced in the primary population by a nominal
stressor can lead to the mimicking of such effects in
a non-exposed bystander population that is optically-
coupled to the former biosystem. It is thus logical to
suggest that the observation of mirroring effects
would be expected in bystander cultures exposed to
biophotons produced secondarily to insult of a pri-
mary culture by any biological stressor, particularly
ionizing radiation.
Very recent work by our group confirms that
irradiated cells emit biophotons which can cause
bystander effects in flasks placed on top of the irra-
diated flasks but where no medium contact is
involved. This again confirms that an electromagnetic
signal is involved(36, 37) but the physical processes
involved remain to be elucidated.
3
MECHANISMS INVOLVED IN THE
ELECTROMAGNETIC BYSTANDER EFFECT
CAUSED BY IONIZING RADIATION
The experiments performed by our group strongly
suggest that the mitochondria are critically import-
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ant in the transduction of the ionizing radiation
energy to induce bystander effects(38–43). There is
also considerable evidence that p53 status of the cells
is critical to the mechanism(44–48). Mitochondria are
known to generate ATP for chemical signaling path-
ways(49–51). Recent studies in our laboratory have
demonstrated that the biophotons generated by ion-
izing radiation can completely inhibit complex 1
activity of the OXPHOS pathway with downstream
consequences for ATP synthase activity(52). Coupled
with the work on the production of bystander effect-
inducing exosomes (BEIE) by cells receiving biopho-
tons generated by exposure of physically separated
flasks to ionizing radiation(47) this suggests that sup-
pression of OXPHOS activity leads to release of
BEIE, i.e. exosomes with a different profile from
control exosomes and with an ability to induce a
bystander effect. The suggested mechanism is
depicted in Figure 1.
POTENTIAL TO HARNESS FOR MEDICAL
OR RADIATION PROTECTION PURPOSES
While the mechanisms involved in the generation
and signal transduction of biophotons induced by
ionizing radiation are fascinating, they may have
major relevance in a practical sense for medicine.
The generation of biophotons along a track of ioniz-
ing radiation in a tissue means that in addition to
direct damage along the track, there will be effects
produced by the interaction of the biophotons with
mitochondria or other organelles in cells along the
track and in any cells which received biophoton
energy. Depending on the photon energy, they could
potentially travel distances up to millimeters in the
tissue(53, 54). This effectively produces a bystander
effect in cells in a targeted tissue, which did not
receive a direct ionizing track. Given what we know
about biophoton effects, there could be wide impli-
cations for cellular and tissue level response and
therefore implications in the considerations of
humans and other organisms in radiation protection
policies. There may also be targets for new drugs
which could amplify or suppress these biophoton
effects.
AVENUES FOR FUTURE RESEARCH
The discussion above suggests several avenues for
further research. To date photons collection has
been gated to 340 ± 5 nm wavelengths. However, we
have evidence that photons are emitted along the
 C. MOTHERSILL ET AL.

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Figure 1. The proposed mechanism of action of bystander exosomes. Under controlled conditions, exosomes are released
which do not contain factors that can induce bystander effects in recipient cells. Under biophoton irradiation, signalling
pathways acting downstream of suppressed ATP synthase produce signalling molecules which are packaged in exosomes.
These “bystander exosomes” can be taken up by unirradiated cells and produce bystander effects due to the release of sol-
uble signalling factors; these factors contribute to signalling in bystander-related pathways.

electromagnetic spectrum so it is clearly important CONCLUSIONS

to identify the spectral emission profile. It is also
There is ample evidence since the 1930’s for the
important to discover in our system what is absorb-
emission of biophotons from organic material and
ing the biophotons. Earlier research suggests the
for their biological activity. Recent results suggest
tyrosine and tryptophan are likely candidates but
that they can also be produced following exposure of
these may be more involved in generation of the
cells to ionizing radiation and that in this situation
photons due to excitation decay rather than absorp-
they can induce bystander effects in unirradiated
tion of already generated photons. The factors lead-
cells. The mechanisms by which biophotons produce
ing to the change in exosome profile due to
bystander effects involves mitochondrial OXPHOS,
absorption of the biophotons by cells also need
p53 status and the production of exosomes with
elucidation.

4
 BIOPHOTONS IN RADIOBIOLOGY: INHIBITORS, COMMUNICATORS AND REACTORS
altered profiles. The processes enhance our under-
standing of intercellular communication under
homeostatic and stress conditions.
ACKNOWLEDGEMENTS
The authors acknowledge support from the Natural
Sciences and Engineering Research Council of Canada
(NSERC), Discovery and Collaborative Research and
Development Programmes, the Canada Research
Chairs Programme, CANDU Owner’s Group, Bruce
Power and the National CFIDS (Chronic Fatigue and
Immune Deficiency Syndrome) Foundation, Inc.
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