Protection of microcirculation in rat brain against late radiation injury by gammaphos

Plotnikova, E.; Levitman, M. Kh.; Shaposhnikova, V. V.; Koshevoj, Ju.V.; Eidus, L.Kh.

doi:10.1016/0360-3016(84)90055-5

Cited by 14 publications

(2 citation statements)

References 6 publications

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“…More importantly, treatment of animals with systemic hypoxia com-pletely reversed whole brain radiation-induced impairments in learning and memory (Warrington et al ., 2012). In addition, the radioprotective drug gammaphos (S-2[3-amino propylamino] ethylphosphorothioate) exerted protective effects on cerebro-vascular system though effective prevention of endothelial cell loss in brain (Plotnikova et al ., 1984; Plotnikova et al ., 1988; Lyubimova and Hopewell, 2004). It was also found that less than 10% of animals receiving gammaphos showed brain in-jury such as necrosis, while approximately 50% of the animals that had not received gammaphos exhibited brain injury by 65 weeks after irradiation (Lyubimova and Hopewell, 2004).…”

Section: Radiation Therapy and Brain Injurymentioning

confidence: 99%

Whole Brain Radiation-Induced Cognitive Impairment: Pathophysiological Mechanisms and Therapeutic Targets

Lee¹,

Cho²,

Lee³

et al. 2012

Biomolecules and Therapeutics

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Radiation therapy, the most commonly used for the treatment of brain tumors, has been shown to be of major significance in tu-mor control and survival rate of brain tumor patients. About 200,000 patients with brain tumor are treated with either partial large field or whole brain radiation every year in the United States. The use of radiation therapy for treatment of brain tumors, however, may lead to devastating functional deficits in brain several months to years after treatment. In particular, whole brain radiation therapy results in a significant reduction in learning and memory in brain tumor patients as long-term consequences of treatment. Although a number of in vitro and in vivo studies have demonstrated the pathogenesis of radiation-mediated brain injury, the cel-lular and molecular mechanisms by which radiation induces damage to normal tissue in brain remain largely unknown. Therefore, this review focuses on the pathophysiological mechanisms of whole brain radiation-induced cognitive impairment and the iden-tification of novel therapeutic targets. Specifically, we review the current knowledge about the effects of whole brain radiation on pro-oxidative and pro-inflammatory pathways, matrix metalloproteinases (MMPs)/tissue inhibitors of metalloproteinases (TIMPs) system and extracellular matrix (ECM), and physiological angiogenesis in brain. These studies may provide a foundation for defin-ing a new cellular and molecular basis related to the etiology of cognitive impairment that occurs among patients in response to whole brain radiation therapy. It may also lead to new opportunities for therapeutic interventions for brain tumor patients who are undergoing whole brain radiation therapy.

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Section: Radiation Therapy and Brain Injurymentioning

confidence: 99%

Whole Brain Radiation-Induced Cognitive Impairment: Pathophysiological Mechanisms and Therapeutic Targets

Lee¹,

Cho²,

Lee³

et al. 2012

Biomolecules and Therapeutics

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show abstract

“…Delayed radiation encephalopathy includes parenchymal foci of necrosis, particularly of white matter, or demyelination with rela tive preservation of axons as well as the vasculopathy mentioned above [18][19][20][21][22][23][24], Experimentally, metabolic rates of some brain structures are reduced following moderate doses of x-radiation [25]. Whether or not radi ation leukoencephalopathy is related to vascular abnor malities, a number of reports have appeared suggesting that protection of the microcirculation may be possible [26] . In our case, perivascular fibrosis in the field of overlap of the two lateral radiation portals is by far the predominant abnormality.…”

Section: Discussionmentioning

confidence: 99%