Journal of Radiation Research 

About: Journal of Radiation Research is an academic journal published by Oxford University Press. The journal publishes majorly in the area(s): Medicine & Radiation therapy. It has an ISSN identifier of 0449-3060. It is also open access. Over the lifetime, 3647 publications have been published receiving 55615 citations. The journal is also known as: JRR.

Radioprotectors in radiotherapy.

Abstract: Radiation Biology Division, Bhabha Atomic Research Centre, Mumbai 400 085, Department of Radiotherapy, All India Institute of Medical Sciences, New Delhi 110 029, India and Department of Radiation Biology and Medical Genetics, Graduate School of Medicine, Osaka University, B4, 2–2 Yamada-oka, Suita, Osaka 565–0871, Japan (Received, May 25, 2000) (Revision received, Novemver 24, 2000) (Accepted, December 7, 2000)

The mechanisms of UV mutagenesis.

Abstract: Ultraviolet (UV) light induces specific mutations in the cellular and skin genome such as UV-signature and triplet mutations, the mechanism of which has been thought to involve translesion DNA synthesis (TLS) over UV-induced DNA base damage. Two models have been proposed: "error-free" bypass of deaminated cytosine-containing cyclobutane pyrimidine dimers (CPDs) by DNA polymerase η, and error-prone bypass of CPDs and other UV-induced photolesions by combinations of TLS and replicative DNA polymerases--the latter model has also been known as the two-step model, in which the cooperation of two (or more) DNA polymerases as misinserters and (mis)extenders is assumed. Daylight UV induces a characteristic UV-specific mutation, a UV-signature mutation occurring preferentially at methyl-CpG sites, which is also observed frequently after exposure to either UVB or UVA, but not to UVC. The wavelengths relevant to the mutation are so consistent with the composition of daylight UV that the mutation is called solar-UV signature, highlighting the importance of this type of mutation for creatures with the cytosine-methylated genome that are exposed to the sun in the natural environment. UVA has also been suggested to induce oxidative types of mutation, which would be caused by oxidative DNA damage produced through the oxidative stress after the irradiation. Indeed, UVA produces oxidative DNA damage not only in cells but also in skin, which, however, does not seem sufficient to induce mutations in the normal skin genome. In contrast, it has been demonstrated that UVA exclusively induces the solar-UV signature mutations in vivo through CPD formation.

Formation of clustered dna damage after high-let irradiation: a review

Abstract: Radiation can cause as well as cure cancer. The risk of developing radiation-induced cancer has traditionally been estimated from cancer incidence among survivors of the atomic bombs in Hiroshima and Nagasaki. These data provide the best estimate of human cancer risk over the dose range for low linear energy transfer (LET) radiations, such as X- or gamma-rays. The situation of estimating the real biological effects becomes even more difficult in the case of high LET particles encountered in space or as the result of domestic exposure to particles from radon gas emitters or other radioactive emitters like uranium-238. Complex DNA damage, i.e., the signature of high-LET radiations comprises by closely spaced DNA lesions forming a cluster of DNA damage. The two basic groups of complex DNA damage are double strand breaks (DSBs) and non-DSB oxidative clustered DNA lesions (OCDL). Theoretical analysis and experimental evidence suggest there is increased complexity and severity of complex DNA damage with increasing LET (linear energy transfer) and a high mutagenic or carcinogenic potential. Data available on the formation of clustered DNA damage (DSBs and OCDL) by high-LET radiations are often controversial suggesting a variable response to dose and type of radiation. The chemical nature and cellular repair mechanisms of complex DNA damage have been much less characterized than those of isolated DNA lesions like an oxidized base or a single strand break especially in the case of high-LET radiation. This review will focus on the induction of clustered DNA damage by high-LET radiations presenting the earlier and recent relative data.

Biological effects of low intensity ultrasound: the mechanism involved, and its implications on therapy and on biosafety of ultrasound.

Abstract: The biological effects of low intensity ultrasound (US) in vitro; the mechanisms involved; and the factors that can enhance or inhibit these effects are reviewed. The lowest possible US intensities required to induce cell killing or to produce free radicals were determined. Following sonication in the region of these intensities, the effects of US in combination with either hyperthermia, hypotonia, echo-contrast agents (ECA), CO2, incubation time, high cell density or various agents were examined. The results showed that hyperthermia, hypotonia and microbubbles are good enhancers of the bioeffects, while CO2, incubation time and high cell density are good inhibitors. Cellular membrane damage is pivotal in the events leading to cell death, with the cellular damage-and-repair mechanism as an important determinant of the fate of the damaged cells. The optimal level of apoptosis (with minimal lysis) and optimal gene transfection efficiency were attained using a pulsed low intensity US. In summary, the findings suggest that low intensity US is potentially useful in therapy, while on the other hand, they also call for further investigation of such clinical scenarios as high-grade fever, edema or use of ECA which may lead to the lowering of the threshold for bioeffects with diagnostic US.

Studies on Biological Effects of Ion Beams on Lethality, Molecular Nature of Mutation, Mutation Rate, and Spectrum of Mutation Phenotype for Mutation Breeding in Higher Plants

Abstract: Recently, heavy ions or ion beams have been used to generate new mutants or varieties, especially in higher plants. It has been found that ion beams show high relative biological effectiveness (RBE) of growth inhibition, lethality, and so on, but the characteristics of ion beams on mutation have not been clearly elucidated. To understand the effect of ion beams on mutation induction, mutation rates were investigated using visible known Arabidopsis mutant phenotypes, indicating that mutation frequencies induced by carbon ions were 20-fold higher than by electrons. In chrysanthemum and carnation, flower-color and flower-form mutants, which are hardly produced by gamma rays or X rays, were induced by ion beams. Novel mutants and their responsible genes, such as UV-B resistant, serrated petals and sepals, anthocyaninless, etc. were induced by ion beams. These results indicated that the characteristics of ion beams for mutation induction are high mutation frequency and broad mutation spectrum and therefore, efficient induction of novel mutants. On the other hand, PCR and sequencing analyses showed that half of all mutants induced by ion beams possessed large DNA alterations, while the rest had point-like mutations. Both mutations induced by ion beams had a common feature that deletion of several bases were predominantly induced. It is plausible that ion beams induce a limited amount of large and irreparable DNA damage, resulting in production of a null mutation that shows a new mutant phenotype.