Effect of X-Radiation on the Flow of Perfusion Fluid Through the Isolated Rabbit's Ear

Gerstner, Herbert B.; Brooks, Phillips M.; Smith, Sydney

doi:10.1152/ajplegacy.1955.182.3.459

Cited by 8 publications

(2 citation statements)

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“…54,55 Since then a considerable body of accumulated evidence has shown that radiation early destabilizes the plasma membrane of a range of cell types including the vascular endothelium. 3,56 Cranial irradiation has reduced endothelial cell density in rat brains within a day of 5-200 Gy, and this dose-independent loss persisted for one month after exposure, followed by a slow dose-independent decrease in cell number for 6 months, and thereafter the cell population remained depleted.…”

Section: Early Radiation Induced Cns Abnormalities In Preclinicalmentioning

confidence: 99%

Mechanisms of radiotherapy-associated cognitive disability in patients with brain tumours

et al. 2016

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Standard treatment of primary and metastatic brain tumors includes high dose megavoltage radiation to the cranial vault. About half of patients survive >6 months, many attain long term control or cure, but 50-90% of survivors overall exhibit disabling cognitive dysfunction. The radiation cognitive syndrome is poorly understood and there is no effective prevention or long-term treatment. Attention has primarily focused on mechanisms of disability appearing at six months to one year after radiotherapy. However, a range of studies have revealed that CNS alterations and dysfunction develop much earlier than 6 months following radiation exposure. This has prompted the recent hypothesis that relatively subtle early forms of radiation induced CNS damage may drive chronic pathophysiology leading to permanent cognitive decline. Within this perspective, the present review presents evidence of acute CNS irradiation triggered inflammation, and injury to neuronal lineages, accessory cells and their progenitors, and loss of supporting structure integrity. Moreover, injury related processes set in motion soon after intracranial irradiation may interact and synergize to alter the neuronal and supporting cell progenitor signaling environment in stem cell niches in the brain, and specifically in the hippocampus, a structure critical to memory and cognition. Changed niche conditions may cause a sustained decline in neurons and progressive deterioration of cognition. The concluding discussion addresses, (1) what further data is needed, and (2) potential treatment interventions, identified via recent findings on acute CNS radiation injury, that may reverse degenerative processes before they can cause permanent cognitive disability.

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Section: Early Radiation Induced Cns Abnormalities In Preclinicalmentioning

confidence: 99%

Mechanisms of radiotherapy-associated cognitive disability in patients with brain tumours

et al. 2016

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“…Among these changes, radiation-induced alterations in vascular cell population may contribute to the occurrence of RIND via two mechanisms. First, it has long been recognized that vascular disruption can be induced quickly (within hours) by a single dose of radiation, followed by vascular dysfunction several months later [ 23 , 24 ]. Further studies revealed that irradiation can cause significant endothelial cell loss through apoptosis within a day, which persists for months [ 25–27 ].…”

Section: Discussionmentioning

confidence: 99%

Irradiated microvascular endothelial cells may induce bystander effects in neural stem cells leading to neurogenesis inhibition

Zhang

et al. 2022

Journal of Radiation Research

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Radiation-induced neurocognitive dysfunction (RIND) has attracted a lot of attention lately due to the significant improvement of the survival of cancer patients after receiving cranial radiotherapy. The detailed mechanisms are not completely understood, but extensive evidence supports an involvement of the inhibition of hippocampal neurogenesis, which may result from radiation-induced depletion of neural stem cells (NSCs) as well as the damage to neurogenic niches. As an important component of neurogenic niches, vascular cells interact with NSCs through different signaling mechanisms, which is similar to the characteristics of radiation-induced bystander effect (RIBE). But whether RIBE is involved in neurogenesis inhibition contributed by the damaged vascular cells is unknown. Thus, the purpose of the present study was to investigate the occurrence of RIBEs in non-irradiated bystander NSCs induced by irradiated bEnd.3 vascular endothelial cells in a co-culture system. The results show that compared with the NSCs cultured alone, the properties of NSCs were significantly affected after co-culture with bEnd.3 cells, and further change was induced without obvious oxidative stress and apoptosis when bEnd.3 cells were irradiated, manifesting as a reduction in the proliferation, neurosphere-forming capability and differentiation potential of NSCs. All these results suggest that the damaged vascular endothelial cells may contribute to neurogenesis inhibition via inducing RIBEs in NSCs, thus leading to RIND.

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The Effects of Ionizing Radiation on the Nervous System

Gangloff¹,

Hug²

1965

Advances in Biological and Medical Physics

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Effect of X-Radiation on the Flow of Perfusion Fluid Through the Isolated Rabbit's Ear

Cited by 8 publications

References 0 publications

Mechanisms of radiotherapy-associated cognitive disability in patients with brain tumours

Mechanisms of radiotherapy-associated cognitive disability in patients with brain tumours

Irradiated microvascular endothelial cells may induce bystander effects in neural stem cells leading to neurogenesis inhibition

The Effects of Ionizing Radiation on the Nervous System

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