Cadmium (Cd) is a toxic metal, targeting the lung, liver, kidney, and testes following acute intoxication, and causing nephrotoxicity, immunotoxicity, osteotoxicity and tumors after prolonged exposures. Reactive oxygen species (ROS) are often implicated in Cd toxicology. This minireview focused on direct evidence for the generation of free radicals in intact animals following acute Cd overload and discussed the association of ROS in chronic Cd toxicity and carcinogenesis. Cd-generated superoxide anion, hydrogen peroxide, and hydroxyl radicals in vivo have been detected by the electron spin resonance spectra, which are often accompanied by activation of redox sensitive transcription factors (e.g., NF-κB, AP-1 and Nrf2) and alteration of ROS-related gene expression. It is generally agreed upon that oxidative stress plays important roles in acute Cd poisoning. However, following long-term Cd exposure at environmentally-relevant low levels, direct evidence for oxidative stress is often obscure. Alterations in ROS-related gene expression during chronic exposures are also less significant compared to acute Cd poisoning. This is probably due to induced adaption mechanisms (e.g, metallothionein and glutathione) following chronic Cd exposures, which in turn diminish Cd-induced oxidative stress. In chronic Cd-transformed cells, less ROS signals are detected with fluorescence probes. Acquired apoptotic tolerance renders damaged cells to proliferate with inherent oxidative DNA lesions, potentially leading to tumorigenesis. Thus, ROS are generated following acute Cd overload and plays important roles in tissue damage. Adaptation to chronic Cd exposure reduces ROS production, but acquired Cd tolerance with aberrant gene expression plays important roles in chronic Cd toxicity and carcinogenesis.

Mycobacterium tuberculosis (Mtb)4 infects one-third of the human population and is the leading cause of lethal bacterial infections worldwide. Synergy of Mtb with the HIV virus and the emergence of extensively drug-resistant Mtb strains (XDR-TB) have further emphasized this pathogen as a major global health threat (1). However, understanding of many of its key physiological processes, particularly those contributing to intracellular survival, is limited. One element of Mtb physiology that may prove important for therapeutic development is its unusually high number of cytochromes P450 (P450s). P450s are heme-dependent mono-oxygenases that utilize reducing equivalents from NAD(P)H relayed via electron transfer proteins to activate heme-bound O 2 . Typical of actinomycete genomes, that of Mtb includes 20 genes encoding P450s (2). In these bacteria, P450s are typically involved in the initial catabolism of growth substrates and in secondary metabolite biosynthesis. Given the high number of P450s in Mtb and their susceptibility to azole drugs, this class of enzyme has been proposed as a promising target for antimycobacterial therapeutic development (2). However, the function of most mycobacterial P450s has yet to be determined.The gene encoding one Mtb P450, cyp125 (Rv3545c), belongs to a large cluster of genes encoding cholesterol degradation (3). This cluster is conserved in several actinobacteria including the non-pathogenic soil bacterium, Rhodococcus jostii RHA1. The genes encode functions necessary for cholesterol import (4), as well as for the degradation of the steroid side chain and rings A and B (3). Several of the ring degradation enzymes from Mtb have been characterized biochemically (5-9). Animal infection studies of mutants deficient in cholesterol uptake and catabolism have indicated that cholesterol metabolism in Mtb plays an important role in infection, contributing to both dissemination in the host (7) and persistence (9, 10). These results are consistent with several mutant screens, which previously identified numerous genes in the cholesterol degradation pathway as having an impact on intracellular growth and survival in both mouse and macrophage models (11, 12), implicating cholesterol catabolism in Mtb pathogenicity.Cyp125 has been implicated in the in vivo survival of Mtb, although its catalytic activity has not been demonstrated, and its physiological role remains unclear. The cyp125 gene is upregulated during growth of Mtb in interferon ␥-activated macrophages (13)

The Himalaya-Hengduan Mountains encompass two global biodiversity hotspots with high levels of biodiversity and endemism. This area is one of the diversification centres of the genus Rhododendron, which is recognized as one of the most taxonomically challenging plant taxa due to recent adaptive radiations and rampant hybridization. In this study, four DNA barcodes were evaluated on 531 samples representing 173 species of seven sections of four subgenera in Rhododendron, with a high sampling density from the Himalaya-Hengduan Mountains employing three analytical methods. The varied approaches (nj, pwg and blast) had different species identification powers with blast performing best. With the pwg analysis, the discrimination rates for single barcodes varied from 12.21% to 25.19% with ITS < rbcL < matK < psbA-trnH. Combinations of ITS + psbA-trnH + matK and the four barcodes showed the highest discrimination ability (both 41.98%) among all possible combinations. As a single barcode, psbA-trnH performed best with a relatively high performance (25.19%). Overall, the three-marker combination of ITS + psbA-trnH + matK was found to be the best DNA barcode for identifying Rhododendron species. The relatively low discriminative efficiency of DNA barcoding in this genus (~42%) may possibly be attributable to too low sequence divergences as a result of a long generation time of Rhododendron and complex speciation patterns involving recent radiations and hybridizations. Taking the morphology, distribution range and habitat of the species into account, DNA barcoding provided additional information for species identification and delivered a preliminary assessment of biodiversity for the large genus Rhododendron in the biodiversity hotspots of the Himalaya-Hengduan Mountains.