Leukocyte and lymphocyte: Cytotoxicity.

Leukocyte and
Lymphocyte: Acute
Radiation Cytotoxicity.
DMITRI POPOV
MEDICAL DOCTOR ( RUSSIA)
PHD, RADIOBIOLOGY. ADVANCED MEDICAL TECHNOLOGY AND SYSTEMS. (CANADA).

Leukocyte and Lymphocyte
The complicated story about two brothers - Lymphocyte and Leukocyte, and
their terrible relationships with their Uncle Radiation.

Leukocyte and Lymphocyte
 Implications for immune-prophylaxis and immune-therapy of Acute
Radiation Disease.

Leukocyte and Lymphocyte.
 White blood cells (WBCs), also called leukocytes are the cells of
the immune system that are involved in protecting the body against both
infectious disease and foreign invaders or physical factors or cancer. All
leukocytes are produced and derived from a multipotent cell in the bone
marrow known as a hematopoietic stem cell. Leukocytes are found
throughout the body, including the blood and lymphatic system.
 White cells are best classified into two major line-ages: the myeloid
leukocytes and the lymphocytes.
 Maton, D., Hopkins, J., McLaughlin, Ch. W., Johnson, S., Warner, M. Q.,
LaHart, D., & Wright, J. D., Deep V. Kulkarni (1997). Human Biology and
Health. Englewood Cliffs, New Jersey, US: Prentice Hall. ISBN 0-13-981176-
1.

Leukocyte and Lymphocyte: Acute
Radiation Cytotoxicity.
 Polymorphonuclear leukocyte - A type of immune cell that has granules
(small particles) with enzymes that are released during Radiation,
infections, allergic reactions, and asthma. Neutrophils, eosinophils, and
basophils are polymorphonuclear leukocytes. A polymorphonuclear
leukocyte is a type of white blood cell.
 Also called granular leukocyte, granulocyte, and PMN.
 http://www.cancer.gov/publications/dictionaries/cancer-
terms?cdrid=633963

 Polymorphonuclear Leukocytes are one of the main sources of enzymes.
 Enzymes responsible for tissue damages and inflammation development.
Baggiolini et al. 1978.
 Eight acid hydrolases, peroxidase (EC 1.11.1.7), cyanide-insensitive NADH
oxidase and alkaline phosphatase (EC 3.1.3.1.) were demonstrated in
homogenates of human polymorphonuclear leukocytes. Studies on human
polymorphonuclear leukocyte enzymes. I. Assay of acid hydrolases and
other enzymes
 JoséLuis Avila,
 Jacinto Convit

 A low-molecular-weight component of complement, similar to or identical with
human C5a, interacts with human polymorphonuclear leukocytes treated with
cytochalasin B and provokes extracellular release of lysosomal enzymes from
these cells. Enzyme release occurs in the absence of particles and is selective in
that it is not accompanied by release of cytoplasmic enzymes. Ultrastructural
histochemistry of cells exposed to this component of complement revealed
degranulation, fusion of lysosomal with plasma membranes, and transient
assembly of microtubules associated with the release of endogenous
myeloperoxidase. This intracellular events are common to two important
responses of polymorphonuclear leukocytes in inflammation and tissue injury:
(a) release of lysosomal hydrolases and (b) chemotaxis. < Mechanisms of
Lysosomal Enzyme Release from Human Leukocytes: Microtubule Assembly
and Membrane Fusion Induced by a Component of Complement . > Goldstain
I. Proc. Nat. Acad. Sci. USA Vol. 70, No. 10, pp. 2916-2920, October 1973 .

The distribution of peroxidase and six lysosomal enzymes (acid phosphatase,
arylsulfatase, beta-galactosidase, beta-glucuronidase, esterase, and 5'-
nucleotidase) corresponded to that of azurophil granules.
 J Cell Biol. 1968 Nov;39(2):286-98.
 Differences in enzyme content of azurophil and specific granules of
polymorphonuclear leukocytes. I. Histochemical staining of bone marrow
smears.
 Bainton DF, Farquhar MG.

 Polymorphonuclear leukocytes of rabbits and chickens after
homogenization in 0.34 M saccharose or after multiple freezing and
thawing were subjected to differential centrifugation at 150, 800, 10 000
and 50 000 X g. In the fractions obtained in this manner, total bactericidal
activity as well as the activity of myeloperoxidase (E.C. 1. 11. 1. 7), catalase
(E.C. 1.11.1.6), lysozyme (E.C. 3.2.1.17), cathepsin D (E.C. 3.4.4.23) and E,
beta-D-glucuronidase (E.C. 3.2.1.31) and acid phosphatase (E.C. 3.1.3.2)
were determined.
 J Hyg Epidemiol Microbiol Immunol. 1976;20(1):91-100.
 Localization of antibacterial activity and hydrolytic enzymes in subcellular
fractions of rabbit and chicken Polymorphonuclear leukocytes.
 Ferencĭk M, Stefanovic J, Absolonová O, Kotulová D.

 Antibacterial activity was found in all fractions from rabbit leukocytes, but
only in the first fraction from chick leukocytes. The fractions from rabbit
leukocytes contained all enzymes under study while in the fractions from
chicken leukocytes the presence of myeloperoxidase, catalase or cathepsin
E could not be demonstrated. The highest bactericidal activity was found in
the second obtained from the homogenate or rabbit leukocytes.

 The highest specific activity of myeloperoxidase and homogenate of rabbit
leukocytes. The highest specific activity of myeloperoxidase and the lowest
activity of cathepsin D were also demonstrated in this fraction. The
addition of pepstatin to rabbit leukocytes before their disintegration
resulted in the inhibition of the activity of cathepsin D and E and in an
increase in the specific activity of myeloperoxidase as well as in total
bactericidal activity in the individual fractions.

 Phagocytic leukocytes consume oxygen and generate reactive oxygen
species in response to appropriate stimuli. The phagocyte NADPH oxidase,
a multiprotein complex, existing in the dissociated state in resting cells
becomes assembled into the functional oxidase complex upon stimulation
and then generates superoxide anions.
 Reactive oxygen species in phagocytic leukocytes
 John M. Robinson
 Histochem Cell Biol (2008) 130:281–297 DOI 10.1007/s00418-008-0461-4.

 The respiratory burst is mediated by the NADPH-oxidase complex, a
multicomponent system that is rapidly assembled following activation of
neutrophils. As we have discussed previously, the neutrophil NADPH
oxidase produces O2 - and hydrogen peroxide (H2O2) following activation
(Robinson et al. 2004).

 Both H2O2 and O2 - are components of the oxygen-dependent,
antimicrobial system of phagocytic leukocytes (e.g., Robinson and Badwey
1995).
 The cytotoxic effects of O2 - and H2O2 relate to their ability to react with
products of other microbicidal systems or autoimmune reeactions in these
cells to generate additional reactive oxygen species (ROS) [e.g., hydroxyl
radical (OH), singlet oxygen , ozone .
 Superoxide can react with either hypochlorous acid (HOCl) or nitric oxide
(NO) to produce OH
 (Beckman et al. 1990; Ramos et al. 1992).

 Hypochlorous acid and nitric oxide are produced in phagocytic leukocytes
by myeloperoxidase and nitric oxide synthase, respectively (Harrison and
Schultz 1976; Xie et al. 1992).
 Singlet oxygen can form by non enzymatic dismutation of superoxide
(Corey et al. 1987).
 Reactive oxygen species in phagocytic leukocytes
 John M. Robinson

 Highly enriched bovine polymorphonuclear neutrophils (PMN) were able
to destroy herpesvirus-infected cells in the presence of complement. Our
results suggest that some viral antigens are capable of activating the
alternate complement pathway directly which results in cytotoxicity
however, the addition of PMN plus complement resulted in high levels of
cytotoxicity.

 The PMN actively secretes cytolytic substances (Henney, 1975; Sellin,
Wallch & Fischer, 1971) or just allows rearrangement of the target cell
membrane as has been proposed for ADCC and antibodycomplement
mediated lysis (Clark & Klebanoff, 1977; Juy, Billecocq, Faure & Bona, 1977;
Mayer, 1977; Grewal et al., 1980) remains to be determined.

 The evidence from our experiments would appear to suggest the latter
since cell-free supernatants from the cultures were inactive in CDNC and
secondly direct contact between the PMN and target cell was required for
cytotoxicity to occur.
 Immunology 198040 151
 Complement-dependent, polymorphonuclear neutrophil-mediated
cytotoxicity of herpesvirus-infected cells: possible mechanism(s)
ofcytotoxicity
 A. S. GREWAL & L. A. BABIUK Department ofVeterinary Microbiology,
Western CollegeofVeterinary Medicine, University ofSaskatchewan,
Saskatoon, Canada

 Mature natural killer (NK) cells use Ca 2 + -dependent granule exocytosis and
release of cytotoxic proteins, Fas ligand (FasL), and membrane-bound or
secreted cytokines (tumor necrosis factor [TNF] a ) to induce target cell death.
Fas belongs to the TNF receptor family of molecules, containing a conserved
intracytoplasmic “death domain” that indirectly activates the caspase
enzymatic cascade and ultimately apoptotic mechanisms in numerous cell
types. Two additional members of this family, DR4 and DR5, transduce
apoptotic signals upon binding soluble TNF-related apoptosis-inducing ligand
(TRAIL) that, like FasL, belongs to the growing TNF family of molecules.
 Natural Killer (NK) Cell–mediated Cytotoxicity: Differential Use of TRAIL and Fas
Ligand by Immature and Mature Primary Human NK Cells By Loris Zamai,
Manzoor Ahmad, Ian M. Bennett, Livio Azzoni, Emad S. Alnemri, and Bice
Perussia
 From the Jefferson Medical College, Department of Microbiology and
Immunology, Kimmel Cancer Institute, Philadelphia, Pennsylvania 19107

 Unseparated peripheral blood leukocytes obtained from patients with
rheumatoid arthritis (RA) were cytotoxic for synovial cells. The cytotoxic
reactions produced by RA leukocytes were more frequent and of greater
magnitude than cytotoxicity induced by leukocytes from normal persons
and patients with other diseases, primarily connective tissue diseases.
 The Cytotoxicity of Leukocytes and Lymphocytes from
 Patients with Rheumatoid Arthritis for Synovial Cells
 DoNALD A. PERSON, JoH T. SHAP, and MAIRN D. LIDSKY
 From the Departments of Internal Medicine and Virology and
Epidemiology, Baylor College of Medicine, Houston, Texas 77030

The human leukocyte antigen (HLA) system is the locus of genes that encode
for proteins on the surface of cells that are responsible for regulation of
the immune system in humans.
The HLA genes are the human versions of the major histocompatibility
complex (MHC) genes that are found in most vertebrates (and thus are the
most studied of the MHC genes.

 HLAs corresponding to MHC class I (A, B, and C) present peptides from inside
the cell. For example, if the cell is infected by a virus, the HLA system brings
fragments of the virus to the surface of the cell so that the cell can be
destroyed by the immune system. These peptides are produced from digested
proteins that are broken down in the proteasomes. In general, these particular
peptides are smallpolymers, about 9 amino acids in length.[citation needed] Foreign
antigens presented by MHC class I attract killer T-cells (also called CD8positive-
or cytotoxic T-cells) that destroy cells.
 HLAs corresponding to MHC class II (DP, DM, DOA, DOB, DQ, and DR) present
antigens from outside of the cell to T-lymphocytes. These particular antigens
stimulate the multiplication of T-helper cells, which in turn stimulate antibody-
producing B-cells to produce antibodies to that specific antigen. Self-antigens
are suppressed by regulatory T cells.
 HLAs corresponding to MHC class III encode components of the complement
system.

 When a foreign pathogen enters the body, specific cells called antigen-
presenting cells (APCs) engulf the pathogen through a process
called phagocytosis. Proteins from the pathogen are digested into small
pieces (peptides) and loaded onto HLA antigens (to be specific, MHC class
II). They are then displayed by the antigen-presenting cells to T cells, which
then produce a variety of effects to eliminate the pathogen.
 Through a similar process, proteins (both native and foreign, such as the
proteins of virus) produced inside most cells are displayed on HLAs (to be
specific, MHC class I) on the cell surface. Infected cells can be recognized
and destroyed by CD8+ T cells.

 Any cell displaying some other HLA type is "non-self" and is seen as an
invader by the body's immune system, resulting in the rejection of the
tissue bearing those cells. This is particularly important in the case of
transplanted tissue, because it could lead to transplant rejection. Because
of the importance of HLA in transplantation, the HLA loci are some of the
most frequently typed by serology and PCR.

 HLA types are inherited, and some of them are connected
with autoimmune disorders and other diseases.

 Scientists at the Stanford University School of Medicine found that
"Ionizing radiation can functionally alter the immune system and break
self-tolerance"(a technical term for when radiation breaks down the
normal ability to fight off disease). The study is published in the Journal of
Immunology. The researchers irradiated the thymus and the peripheral
lymphoid organs/tissues in mice to induce the autoimmune response.
Total lymphoid irradiation on mice caused various organ-specific
autoimmune diseases, such as gastritis, thyroiditis, and orchitis, depending
on the radiation dosages, the extent of lymphoid irradiation, and the
genetic background of the mouse strains. They concluded, "these results
indicate that high dose, fractionated ionizing radiation on the lymphoid
organs/tissues can cause autoimmune disease by affecting the T cell
immune system."

 A lymphocyte is one of the subtypes of white blood cell in
a vertebrate's immune system. They include natural killer cells (NK cells)
(which function in cell-mediated, cytotoxic innate immunity), T
cells (for cell-mediated, cytotoxic adaptive immunity), and B cells (for
humoral, antibody-driven adaptive immunity).

 Cell mediated immunity is an immune response that does not
involve antibodies, but rather involves the activation
of phagocytes, antigen-specific cytotoxic T-lymphocytes, and the release of
various cytokines in response to an antigen. Historically, the immune
system was separated into two branches: humoral immunity, for which the
protective function of immunization could be found in the humor (cell-free
bodily fluid or serum) and cellular immunity, for which the protective
function of immunization was associated with cells. CD4 cells or helper T
cells provide protection against different pathogens. Cytotoxic T cells
cause death by apoptosis without using cytokines, therefore in cell-
mediated immunity cytokines are not always present.

 Cellular immunity protects the body by:
 activating antigen-specific cytotoxic T-lymphocytes that are able to
induce apoptosis/ necrosis in body cells displaying epitopes of foreign
antigen on their surface, such as virus-infected cells, cells with intracellular
bacteria, autoimmune cells, irradiated cells, isolated from irradiated
mammals, and cancer cells displaying tumor antigens;
 activating macrophages and natural killer cells, enabling them to destroy
pathogens; and
 stimulating cells to secrete a variety of cytokines that influence the
function of other cells involved in adaptive immune responses and innate
immune responses.

 A cytotoxic T cell (also known as TC, cytotoxic T lymphocyte, CTL, T-killer cell, cytolytic T cell,
CD8+ T-cells or killer T cell) is a T lymphocyte (a type of white blood cell) that kills cancer cells,
cells that are infected (particularly with viruses), or cells that are damaged in other ways for
example by radiation.
 Most cytotoxic T cells express T-cell receptors (TCRs) that can recognize a specific antigen. An
antigen is a molecule capable of stimulating an immune response, and is often produced by
cancer cells or viruses. Antigens inside a cell are bound to class I MHC molecules, and brought
to the surface of the cell by the class I MHC molecule, where they can be recognized by the T
cell. If the TCR is specific for that antigen, it binds to the complex of the class I MHC molecule
and the antigen, and the T cell destroys the cell.
 In order for the TCR to bind to the class I MHC molecule, the former must be accompanied by
a glycoprotein called CD8, which binds to the constant portion of the class I MHC molecule.
Therefore, these T cells are called CD8+ T cells.
 The affinity between CD8 and the MHC molecule keeps the TC cell and the target cell bound
closely together during antigen-specific activation. CD8+ T cells are recognized as TC cells
once they become activated and are generally classified as having a pre-defined cytotoxic role
within the immune system. However, CD8+ T cells also have the ability to make
some cytokines.

 With an exception of some cell types, such as non-nucleated cells
(including erythrocytes), Class I MHC is expressed by all host cells. When
these cells are infected with a virus(or another intracellular pathogen), the
cells degrade foreign proteins via antigen processing. These result in
peptide fragments, some of which are presented by MHC Class I to the T
cell antigen receptor (TCR) on CD8+ T cells.
 The activation of cytotoxic T cells is dependent on several simultaneous
interactions between molecules expressed on the surface of the T cell and
molecules on the surface of the antigen-presenting cell (APC). For instance,
consider the two signal model for TC cell activation.

 First Signal – TCR - peptide-bound MHC class I molecule - There is a
second interaction between the CD8 co-receptor and the class I MHC
molecule to stabilize this signal.
 Second Signal - CD28 molecule on the T cell - either CD80 or CD86 (also
called B7-1 and B7-2) - CD80 and CD86 are known as costimulators for T
cell activation. This second signal can be assisted (or replaced) by
stimulating the TC cell with cytokines released from helper T cells.

 A simple activation of naive CD8+ T cells requires the interaction with
professional antigen-presenting cells, mainly with matured dendritic cells.
To generate longlasting memory T cells and to allow repetitive stimulation
of cytotoxic T cells, dendritic cells have to interact with both, activated
CD4+ helper T cells and CD8+ T cells.[1][2] During this process, the
CD4+ helper T cells "license" the dendritic cells to give a potent activating
signal to the naive CD8+ T cells.

 While in most cases activation is dependent on TCR recognition of antigen,
alternative pathways for activation have been described. For example,
cytotoxic T cells have been shown to become activated when targeted by
other CD8 T cells leading to tolerization of the latter.
 Once activated, the TC cell undergoes clonal expansion with the help of the
cytokine Interleukin-2 (IL-2), which is a growth and differentiation factor
for T cells. This increases the number of cells specific for the target antigen
that can then travel throughout the body in search of antigen-
positive somatic cells.

 When exposed to infected/dysfunctional somatic cells, TC cells release the
cytotoxins perforin, granzymes, and granulysin.
 Through the action of perforin, granzymes enter the cytoplasm of the
target cell and their serine protease function triggers the caspase cascade,
which is a series of cysteine proteases that eventually lead
to apoptosis(programmed cell death).

 A second way to induce apoptosis is via cell-surface interaction between the
TC and the infected cell. When a TC is activated it starts to express the surface
protein FAS ligand(FasL)(Apo1L)(CD95L), which can bind to Fas (Apo1)(CD95)
molecules expressed on the target cell. However, this Fas-Fas ligand interaction
is thought to be more important to the disposal of unwanted T
lymphocytes during their development or to the lytic activity of certain TH cells
than it is to the cytolytic activity of TC effector cells. Engagement of Fas with
FasL allows for recruitment of the death-induced signaling complex (DISC). The
Fas-associated death domain (FADD) translocates with the DISC, allowing
recruitment of procaspases 8 and 10. These caspases then activate the effector
caspases 3, 6, and 7, leading to cleavage of death substrates such as lamin A,
lamin B1, lamin B2, PARP (poly ADP ribose polymerase), and DNAPK (DNA-
activated protein kinase). The final result is apoptosis of the cell that expressed
Fas.

 One of the functions of the immune system is to recognize and destroy
abnormal or infected cells to maintain homeostasis. This is accomplished
by cytotoxic lymphocytes. Cytotoxicity is a highly organized multifactor
process. Here, we reviewed the apoptosis pathways induced by the two
main cytotoxic lymphocyte subsets, natural killer (NK) cells and CD8+ T
cells. In base to recent experimental evidence, we reviewed NK receptors
involved in recognition of target-cell, as well as lytic molecules such as
perforin, granzymes-A and -B, and granulysin.
 Cell Mol Immunol. 2009 Feb;6(1):15-25. doi: 10.1038/cmi.2009.3.
 Cell death mechanisms induced by cytotoxic lymphocytes.
 Chávez-Galán L1, Arenas-Del Angel MC, Zenteno E, Chávez R, Lascurain R.

 Granulysin is a human cytolytic molecule present in cytotoxic granules with
perforin and granzymes. Recombinant 9-kDa granulysin kills a variety of
microbes, including bacteria, yeast, fungi, and parasites, and induces
apoptosis in tumor cells by causing intracellular calcium overload,
mitochondrial damage, and activation of downstream caspases.
 J Immunol. 2011 Mar 15;186(6):3497-504. doi: 10.4049/jimmunol.1003409.
Epub 2011 Feb 4.
 Granulysin delivered by cytotoxic cells damages endoplasmic reticulum and
activates caspase-7 in target cells.
 Saini RV1, Wilson C, Finn MW, Wang T, Krensky AM, Clayberger C.

 Cytotoxic T lymphocytes (CTLs) provide potent defences against virus
infection and intracellular pathogens. However, CTLs have a dark side —
their lytic machinery can be directed against selftissues in autoimmune
disorders, transplanted cells during graft rejection and host tissues to
cause graft-versus-host disease, which is one of the most serious diseases
related to CTL function. Although this duplicitous behaviour might seem
contradictory, both beneficial and detrimental effects are the result of the
same effector proteins. So, an understanding of the mechanisms that are
used by CTLs to destroy targets and a knowledge of pathogen
immuneevasion strategies will provide vital information for the design of
new therapies. CYTOTOXIC T LYMPHOCYTES: ALL ROADS LEAD TO DEATH
Michele Barry* and R. Chris Bleackley‡

 Cytotoxic T lymphocytes mediate lysis of target cells by various
mechanisms, including exocytosis of lytic proteins (perforin, granzymes)
and receptor-ligand binding of Fas/APO molecules. Death of target cells is
characterized by either necrosis or apoptosis, depending on the killing
mechanism used and on the metabolism of the target cell itself.
 Killing Mechanisms of Cytotoxic T Lymphocytes
 Peter Groscurth, Luis Filgueira
 Physiology Published 1 February 1998 Vol. 13 no. 1, 17-21 DOI:

 The lysis of target cells via CTL proceeds through a sequence of
programmed steps, including killer-target cell binding, delivery of the
lethal hit, target cell lysis, and killer cell recycling. After recognition of the
appropriate antigen, the CTL bind firmly to the surface of the target cell, an
event that depends on the presence of Mg2+ but not Ca2+. The subsequent
lysis of the target cells is mediated by two different mechanisms:
exocytosis of lytic proteins and/or receptor-ligand binding of Fas/APO
molecules.
 The various pathways may result in different types of target cell death:
necrosis and apoptosis.
 http://physiologyonline.physiology.org/content/13/1/17

 Lysosomes of CTL have a unique morphology that can be seen only by
electron microscopy . Each granule has an electron-dense core surrounded
by small, round vesicles. Within the core, several types of lytic proteins are
stored in an inactive form. Upon binding of the effector cell to the target
cell, the lysosomes are directed toward the contact area by reorientation of
the microtubule organization center. Subsequently, the content of the
granules is released into the intercellular space via exocytosis. Cytolysis of
target cell is then mediated by two types of lytic proteins, perforin and
granzymes, that act either alone or in combination with each other.
 http://physiologyonline.physiology.org/content/13/1/17

 In cancer patients undergoing radiation therapy, the beneficial effects of radiation can
extend beyond direct cytotoxicity to tumor cells. Delivery of localized radiation to
tumors often leads to systemic responses at distant sites, a phenomenon known as the
abscopal effect which has been attributed to the induction and enhancement of the
endogenous anti-tumor innate and adaptive immune response. The mechanisms
surrounding the abscopal effect are diverse and include trafficking of lymphocytes into
the tumor microenvironment, enhanced tumor recognition and killing via up-regulation
of tumor antigens and antigen presenting machinery and, induction of positive
immunomodulatory pathways. Here, we discuss potential mechanisms of radiation-
induced enhancement of the anti-tumor response through its effect on the host
immune system and explore potential combinational immune-based strategies such as
adoptive cellular therapy using ex vivo expanded NK and T cells as a means of delivering
a potent effector population in the context of radiation-enhanced anti-tumor immune
environment.
 The Effect of Radiation on the Immune Response to Cancers Bonggoo Park 1 , Cassian
Yee 2 and Kyung-Mi Lee 1,*

 http://www.intechopen.com/books/current-topics-in-ionizing-radiation-
research/radiation-toxins-molecular-mechanisms-of-toxicity-and-
radiomimetic-properties-
 Acute Radiation Disease (ARD) or Acute Radiation Syndromes (ARS) are
defined as the collective toxic clinical states observed from the acute
pathological processes in various doses of irradiated mammals; to include:
systemic inflammatory response syndrome (SIRS), toxic multiple organ injury
(TMOI), toxic multiple organ dysfunction syndromes (TMODS), and finally, toxic
multiple organ failure (TMOF). Moderate and high doses of radiation induces
necrosis of radiosensitive cells with the subsequent formation of radiation
toxins and their induced acute inflammatory processes. Radiation necrosis is
the most substantial and most severe form of radiation induced injury, and
when widespread, has grave therapeutic implications . Low doses of radiation
exposure induces apoptosis (controlled, programmed death of radiosensitive
cells) without significant levels of specific radiation-induced toxin formation
and with only low levels of inflammatory response

Leukocyte and lymphocyte: Cytotoxicity.

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