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Developments in understanding agents having activity for the prevention and treatment of radiation injuries are discussed. Chemical radioprotectors have long been dominated by thiol compounds and their phosphorothioate derivatives. Advances have been made to understanding the fundamental mechanisms by which these agents protect against cell killing. The finding that thiols also protect against radiation‐induced mutations and transformation has generated considerable interest. Mutations may be expressed as undesirable late effects in radiotherapy. Such effects are reviewed herein, as is the enormous literature that has accumulated relating to preclinical and clinical studies of the effects of phosphorothioates in animals and humans. A number of nonthiol radioprotective agents, including protease inhibitors, vitamins, metalloelements, and calcium antagonists, are also discussed. There has been a virtual explosion of interest in biological, as opposed to chemical, modifiers of radiation injury. These biologics include cytokines such as interleukin 1 and granulocyte colony‐stimulating factor, eicosanoids such as prostaglandins and leukotrienes, and steroids/glucocorticoids such as dexamethasone and methylprednisolone. In addition, an array of immunomodulatory agents such as glucan and endotoxin have been described, which act by nonspecifically enhancing immunological and hemopoietic responses. Although some of these biologics act best when given prior to irradiation, many of them can modulate radiation injury when given after irradiation, presumably by affecting the recovery and repopulation of critical tissue elements. Biologics thus afford an opportunity for therapeutic intervention following accidental radiation exposure as well as in radiation therapy. Demonstrations of a potential therapeutic advantage from combining chemical radioprotectors, which decrease the extent of initial damage, with nonthiol biologics, which accelerate tissue recovery, provides an attractive approach to radioprotection which also minimizes toxicity.
Developments in understanding agents having activity for the prevention and treatment of radiation injuries are discussed. Chemical radioprotectors have long been dominated by thiol compounds and their phosphorothioate derivatives. Advances have been made to understanding the fundamental mechanisms by which these agents protect against cell killing. The finding that thiols also protect against radiation‐induced mutations and transformation has generated considerable interest. Mutations may be expressed as undesirable late effects in radiotherapy. Such effects are reviewed herein, as is the enormous literature that has accumulated relating to preclinical and clinical studies of the effects of phosphorothioates in animals and humans. A number of nonthiol radioprotective agents, including protease inhibitors, vitamins, metalloelements, and calcium antagonists, are also discussed. There has been a virtual explosion of interest in biological, as opposed to chemical, modifiers of radiation injury. These biologics include cytokines such as interleukin 1 and granulocyte colony‐stimulating factor, eicosanoids such as prostaglandins and leukotrienes, and steroids/glucocorticoids such as dexamethasone and methylprednisolone. In addition, an array of immunomodulatory agents such as glucan and endotoxin have been described, which act by nonspecifically enhancing immunological and hemopoietic responses. Although some of these biologics act best when given prior to irradiation, many of them can modulate radiation injury when given after irradiation, presumably by affecting the recovery and repopulation of critical tissue elements. Biologics thus afford an opportunity for therapeutic intervention following accidental radiation exposure as well as in radiation therapy. Demonstrations of a potential therapeutic advantage from combining chemical radioprotectors, which decrease the extent of initial damage, with nonthiol biologics, which accelerate tissue recovery, provides an attractive approach to radioprotection which also minimizes toxicity.
Various approaches have been developed for diminishing the effects of radiation on normal tissues or enhancing tumor cell killing by ionizing radiation. An important potential use for these agents is to modify the outcome of radiation therapy. Potential radioprotectors or radiosensitizers are organized in this review according to mechanism of action. Most of the agents studied are believed to act by reacting with DNA radicals that are produced within milliseconds of exposure to ionizing radiation. According to this mechanism, protectors restore a single electron to electron‐deficient radicals, preventing degradation of the structure of DNA, whereas sensitizers, such as molecular oxygen or nitroimidazoles, form adducts with these radicals, resulting in damage fixation. WR2721 (Ethyol) is the best‐characterized chemical radioprotector. Preferential activation of WR2721 in certain normal tissues by removal of a phosphate group provides a rationale for selective protection of these tissues. Cytokines and biological modifiers represent an important emerging class of radioprotectors that may be particularly useful in modifying bone marrow injury. Nitroimidazoles have been the most widely studied chemical radiosensitizers. Although clinical results with nitroimidazoles have not been impressive, the potential for this approach has not been fully explored, given that the doses that can be administered have been limited by drug toxicity and supplemental strategies, such as concurrent depletion of endogenous protectors, have not been explored in the clinic. Modifiers of tumor oxygenation represent an important class of radiosensitizers that are currently generating considerable clinical interest. RSR13, a modifier of the oxygen affinity of hemoglobin, is highlighted as an example of the process of drug development for this type of agent.
Metastases are the consequence of a complicated process in which malignant cells detach from the initial cancerous cells and disseminate to other locations. Few therapy options are available that aim to prevent or counteract metastatic disorders. Identifying novel molecular targets and medications, developing techniques to distribute preexisting chemicals, and combining resources to supervise individualized treatment are all part of this process. Because of its improved sensitivity, accuracy, and multiplexed measurement capacity, nanotechnology has been investigated for the recognition of extracellular cancer biomarkers, cancer cells, and in bioimaging. Nanotechnology is a vast and rapidly expanding field with enormous potential in cancer treatment. Nanoparticles can treat resistant cancers with minimal harm to healthy tissues and organs by targeting cancer stem cells. Nanoparticles can also trigger immune cells, which can help to destroy malignancies. The potential of herbal-based nano formulation as a specialized and high-efficacy therapeutic method, opening the path for future research into the screening and use of herbal nanoparticles for cancer treatment. The possible impacts of nanoparticles in the therapy of metastatic cancer, specifically on cell stability, proliferation suppression, eventual interaction with adhesion molecules, and antiangiogenic activity, are discussed in this paper.
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