Global biodiversity conservation priorities.

The location of and threats to biodiversity are distributed unevenly, so prioritization is essential to minimize biodiversity loss. To address this need, biodiversity conservation organizations have proposed nine templates of global priorities over the past decade. Here, we review the concepts, methods, results, impacts, and challenges of these prioritizations of conservation practice within the theoretical irreplaceability/vulnerability framework of systematic conservation planning. Most of the templates prioritize highly irreplaceable regions; some are reactive (prioritizing high vulnerability), and others are proactive (prioritizing low vulnerability). We hope this synthesis improves understanding of these prioritization approaches and that it results in more efficient allocation of geographically flexible conservation funding.

Use of cytogenetic indicators in radiobiology.

The study of ionising radiation has systematically relied on cytogenetic indicators to evaluate the biological effects and has led to theoretical approaches to explain observations associated with radiation exposure. In many of the early studies on radiobiology, the induction of chromosomal aberrations was the method of choice to evaluate dose-response relationships. But progressively, this and other cytogenetic biomarkers were used to obtain mechanistic insight on the biological effects induced by radiation. This paper attempts to give a view on the use of cytogenetic indicators in the study of various radiation-related phenomena, including radiation dosimetry, mechanisms involved in the various cellular responses to radiation, such as bystander effects, chromosomal instability and adaptive response, as well as DNA repair pathways. One future direction may involve the use of cytogenetic indicators to evaluate various molecular determinants in individuals' susceptibility to radiation, using other techniques such as fluorescence in situ hybridisation (FISH) and linking them to specific gene functions and single nucleotide polymorphisms.

Assessment of the adaptive response induced by quercetin using the MNCB peripheral blood human lymphocytes assay.

Over more than two decades the existence of an adaptive response (AR) has been reported in several cell types and extensively studied with low doses of radiation. Besides radiation, some chemicals [alkylating compounds, mitomycin C (MMC), bleomycin, hydrogen peroxide and metals] may also induce an adaptive response. We have recently reported that the food mutagen quercetin can also induce an adaptive response in V79 Chinese hamster cells. In this work we have studied the effect of low doses of quercetin on the genotoxicity of MMC and bleomycin assessed by the formation of micronuclei in cytokinesis-blocked (MNCB) human peripheral blood lymphocytes. Our results suggest the existence of an AR induced by quercetin in human lymphocytes. Seven of the nine donors studied showed in at least one independent experiment a significant decrease in the frequency of MNCB induced by MMC. The range of these decreases varied between 31 and 58%. In addition, we observed an AR induced by quercetin towards challenging doses of bleomycin. In accordance with other studies with ionizing radiation in which heterogeneity of the AR in the population has been extensively observed, the response here reported also showed some degree of variability between the different donors studied. In view of the results obtained one cannot rule out a possible protective effect of low doses of quercetin leading to adaptation to further exposure to mutagens or carcinogens.

Genotoxicity assessment of aromatic amines and amides in genetically engineered V79 cells.

A genetically engineered V79 cell line expressing rat CYP1A2 and another cell line expressing rat CYP1A2 as well as endogenous acetyltransferase activity, as well as CYP-deficient parental V79 cell lines, were used to assess the genotoxicity of the aromatic amines and amides 2-aminoanthracene, 2-aminofluorene, 2-acetylaminofluorene, 4-acetylaminofluorene and 2-amino-3-methylimidazo[4,5-f]quinoline, with chromosomal aberrations and sister chromatid exchanges as the end-points. None of the test compounds showed a clear effect on the frequency of chromosomal aberrations in any cell line used. Sister chromatid exchanges, however, were induced by 2-aminoanthracene, 2-aminofluorene and 2-acetylaminofluorene in the CYP1A2-proficient cells, but not in the CYP1A2-deficient cells. The presence of acetyltransferase activity enhanced the effect of 2-aminoanthracene, 2-aminofluorene and 2-acetylaminofluorene. 4-Acetylaminofluorene and 2-amino-3-methylimidazo[4,5-f]quinoline did not induce sister chromatid exchanges in the investigated cell lines. The use of cell lines with defined metabolic capabilities seems to be a valuable tool to study specific metabolic pathways important in the activation of procarcinogens.