Ability of Lithium to Accelerate the Recovery of Granulopoiesis after Subacute Radiation Injury

Gallicchio, Vincent S.; Chen, M. G.; Watts, Thomas D.

doi:10.3109/02841868409136034

Cited by 15 publications

(10 citation statements)

References 14 publications

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“…9) However, a relatively lowdose (~2 Gy) of whole body irradiation in experimental animals showed transient damage to immature stem cells in specific tissues, including the skin, intestine and testis. [10][11][12] Irradiation has a variety of effects on both the developing and adult brain, even though the adult brain is less vulnerable to irradiation than other organs. While macroscopic changes involving brain tissue destruction are generally associated with high irradiation doses, 13) less histological injury can occur after relatively low doses, resulting in variable degrees of cognitive impairment in adult mammals.…”

Section: Introductionmentioning

confidence: 99%

Transient Impairment of Hippocampus-dependent Learning and Memory in Relatively Low-Dose of Acute Radiation Syndrome is Associated with Inhibition of Hippocampal Neurogenesis

Kim

Lee

Kang

et al. 2008

JRR

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Neurogenesis in the adult hippocampus, which occurs constitutively, is vulnerable to ionizing radiation. In the relatively low-dose exposure of acute radiation syndrome (ARS), the change in the adult hippocampal function is poorly understood. This study analyzed the changes in apoptotic cell death and neurogenesis in the DGs of hippocampi from adult ICR mice with single whole-body gamma-irradiation using the TUNEL method and immunohistochemical markers of neurogenesis, Ki-67 and doublecortin (DCX). In addition, the hippocampus-dependent learning and memory tasks after single whole-body gamma-irradiation were examined in order to evaluate the hippocampus-related behavioral dysfunction in the relatively low-dose exposure of ARS. The number of TUNEL-positive apoptotic nuclei in the dentate gyrus (DG) was increased 6-12 h after acute gamma-irradiation (a single dose of 0.5 to 4 Gy). In contrast, the number of Ki-67- and DCX-positive cells began to decrease significantly 6 h postirradiation, reaching its lowest level 24 h after irradiation. The level of Ki-67 and DCX immunoreactivity decreased in a dose-dependent manner within the range of irradiation applied (0-4 Gy). In passive avoidance and object recognition memory test, the mice trained 1 day after acute irradiation (2 Gy) showed significant memory deficits, compared with the sham controls. In conclusion, the pattern of the hippocampus-dependent memory dysfunction is consistent with the change in neurogenesis after acute irradiation. It is suggested that a relatively low dose of ARS in adult ICR mice is sufficiently detrimental to interrupt the functioning of the hippocampus, including learning and memory, possibly through the inhibition of neurogenesis.

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Section: Introductionmentioning

confidence: 99%

Transient Impairment of Hippocampus-dependent Learning and Memory in Relatively Low-Dose of Acute Radiation Syndrome is Associated with Inhibition of Hippocampal Neurogenesis

Kim

Lee

Kang

et al. 2008

JRR

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“…Cell culture plates were air-dried and CFU-MIX colonies were stained for the presence of benzidine to identify erythroid cells, acetylcholinesterase activity to identify the presence of megakaryocytes, and specific and nonspe cific esterase activity to identify the presence of myeloid and mono cyte-macrophage cells, respectively. The details for these staining procedures have been published previously [27].…”

Section: Assay For In Vitro Multipotential Mixed Colony (Cfu-mix)mentioning

confidence: 99%

Lithium and Hematopoietic Toxicity

Gallicchio¹

1988

Acta Haematol

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Studies are described that demonstrate the ability of lithium (Li) to enhance total peripheral blood neutrophil, platelet and stem cell (CFU-S, CFU-MIX, CFU-GM and CFU-MEG) populations from mice administered cyclophosphamide (CTX). Mice were preinjected on each of 3 consecutive days with ultrapure lithium carbonate (Li₂CO₃, 35 μg/kg b.w.) before receiving CTX (200 mg/kg, b.w.). Control groups were preinjected with phosphate-buffered saline (PBS) before receiving CTX. On days 1, 5, 7, 14, 21, and 28 following CTX, 3 mice from each group were sacrificed. Peripheral blood was obtained and examined for their packed red cell volume, white blood cell differential and platelet counts. Bone marrow and spleen cells were harvested and assayed for their stem cell content (CFU-S, CFU-MIX, CFU-GM, and CFU-MEG). Mice receiving Li prior to CTX did not develop thrombocytopenia and their absolute granulocyte counts recovered more rapidly when compared to CTX-PBS controls. Li-CTX bone marrow CFU-S and CFU-MIX were not as severely depressed when compared to the CTX-PBS controls. Li-CTX splenic-derived CFU-GM and CFU-MEG were increased significantly when compared to CTX-PBS controls and their rate of recovery was greater than that observed from bone marrow. These results demonstrate and confirm the capability of Li to accelerate hematopoietic recovery following the use of agents known to suppress hematopoiesis.

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“…Among several known radioprotective chemicals, LiCl was selected because of its comparatively low toxic effects in biological systems. There is not much information published on the protective activity of LiCl, and nearly all of it is related to the protection of the hematopoietic system against whole body irradiation [1][2][3][4][5][6][7]. However, according to even contrary findings and from the point of view of cell survival, LiCl as immunomodulator has been reported to accelerate radiation-induced death in ddY mice rather than having any radioprotective effect [12], although very high x-ray doses of 8.5 Gy administered to a special strain of experimental mice was possibly responsible for this adverse effect of LiCl.…”

Section: Discussionmentioning

confidence: 99%

“…In addition, lithium has been reported to have a protective action against acute radiation injury [1]. It has been demonstrated that lithium markedly accelerates the production of hematopoietic cells following total body irradiation.…”

Section: Introductionmentioning

confidence: 99%

“…It has been demonstrated that lithium markedly accelerates the production of hematopoietic cells following total body irradiation. More specifically, it is a stimulator of granulopoiesis, with marked proliferative effects on a number of stem cells and progenitor cell populations of bone marrow [2][3][4][5][6]. This radioprotective action of lithium has also been attributed to the recovery kinetics of one or more factors in the bone marrow precursors [7].…”

Section: Introductionmentioning

confidence: 99%

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Effects of lithium chloride as a potential radioprotective agent on radiation response of DNA synthesis in mouse germinal cells

Bhattacharjee

Rajan

Krishnamoorthy

et al. 1997

Radiation and Environmental Biophysics

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Mouse spermatogonial germ cells are highly sensitive to ionizing radiation. Lithium salts are reported to stimulate the postirradiation recovery of hematopoietic marrow cells. We have, therefore, examined whether administered lithium chloride (LiCl) would also be able to protect the mouse germinal cells against radiation injury. Taking DNA synthesis as an endpoint, our results show that the testicular DNA-specific activity in irradiated mice was higher by 61% on average when they had been pretreated with LiCl both 24 h and 1 h prior to gamma-irradiation (2.0 Gy). It was also observed that the DNA synthetic activity in the germinal cells fully recovered after LiCl pretreatment at doses of 40 mg per kg body weight prior to total body irradiation of 0.05-0.25 Gy, whereas at doses of 0.5-6.0 Gy, following the same procedure of LiCl pretreatment, only an incomplete recovery was observed. The dose reduction factor for LiCl is 1.84. The current findings indicate that pretreatment with LiCl provides considerable protection against radiation damage in mouse spermatogonia.

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Ability of Lithium to Accelerate the Recovery of Granulopoiesis after Subacute Radiation Injury

Cited by 15 publications

References 14 publications

Transient Impairment of Hippocampus-dependent Learning and Memory in Relatively Low-Dose of Acute Radiation Syndrome is Associated with Inhibition of Hippocampal Neurogenesis

Transient Impairment of Hippocampus-dependent Learning and Memory in Relatively Low-Dose of Acute Radiation Syndrome is Associated with Inhibition of Hippocampal Neurogenesis

Lithium and Hematopoietic Toxicity

Effects of lithium chloride as a potential radioprotective agent on radiation response of DNA synthesis in mouse germinal cells

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