Species distribution modelling and cpSSR reveal population history of the Neotropical annual herb Tithonia rotundifolia (Asteraceae).

The impacts of the historical geologic and climatic events on the diversity and genetic structure of Neotropical taxa have recently become a subject of study. However, annual plants associated with tropical dry forests remain under-studied. The exploration of additional taxa in contrasting environments will improve the current understanding of responses of the Neotropical biota to these events. Here, we explore the species distribution and geographic structure of the annual herb Tithonia rotundifolia. We sampled 175 individuals from 19 populations of T. rotundifolia. Species distribution modelling and six microsatellite chloroplast loci were used to infer its population history. We identified areas of historical climate suitability and then tested if there is genetic structuring among these areas. Haplotypes showed strong phylogeographic structure. Historical climatic suitability areas were found along the Pacific coast; however, a gap was found at the Isthmus of Tehuantepec (IT). Although Bayesian analysis showed population structuring, amova revealed that the IT is not its main driver. Instead, a subdivision into a higher number of regions had higher FCT values. Also, populations to the east of the IT showed evidence of recent population expansion and migration in a south-north direction. Pleistocene climate fluctuations partially explain the geographic structure of T. rotundifolia. However, life-history characteristics such as limited seed dispersal and the patchy distribution of suitable habitats explain the high haplotype diversity and population sub-structuring and diversity. Lastly, the absence of geographic structure of some haplotypes may indicate long-distance dispersal, or hybridisation with the closely related T. tubaeformis.

Comparison of two wild rodent species as sentinels of environmental contamination by mine tailings.

BACKGROUND: Contamination with heavy metals is among the most hazardous environmental concerns caused by mining activity. A valuable tool for monitoring these effects is the use of sentinel organisms. Particularly, small mammals living inside mine tailings are an excellent study system because their analysis represents a realistic approach of mixtures and concentrations of metal exposure. PURPOSE: We analyzed metal tissue concentrations and DNA damage levels for comparison between genders of a sentinel (Peromyscus melanophrys) and a nonsentinel (Baiomys musculus) species. Also, the relationship between DNA damage and the distance from the contamination source was evaluated. METHODS: This study was conducted in an abandoned mine tailing at Morelos, Mexico. Thirty-six individuals from both species at the exposed and reference sites were sampled. Metal concentrations in bone and liver of both species were analyzed by atomic absorption spectrophotometry, and DNA damage levels were assayed using the alkaline comet assay. RESULTS: In general, concentrations of zinc, nickel, iron, and manganese were statistically higher in exposed individuals. A significant effect of the organ and the site on all metal tissue concentrations was detected. Significant DNA damage levels were registered in the exposed group, being higher in B. musculus. Females registered higher DNA damage levels than males. A negative relationship between distance from the mine tailing and DNA damage in B. musculus was observed. CONCLUSIONS: We consider that B. musculus is a suitable species to assess environmental quality, especially for bioaccumulable pollutants--such as metals--and recommend that it may be considered as a sentinel species.

Vanadium pentoxide inhalation provokes germinal center hyperplasia and suppressed humoral immune responses.

Vanadium, an important air pollutant derived from fuel product combustion, aggravates respiratory diseases and impairs cardiovascular function. In contrast, its effects on immune response are conflicting. The aim of our work was to determine if spleens of vanadium-exposed CD1 mice showed histological lesions that might result in immune response malfunction. One hundred and twelve CD-1 male mice were placed in an acrylic box and inhaled 0.02 M vanadium pentoxide (V2O5); actual concentration in chamber approximately 1.4 mg V2O5/m(3)) for 1 hr/d, twice a week, for 12 wk. Control mice inhaled only vehicle. Eight mice were sacrificed prior to the exposures. Eight control and eight V2O5-exposed mice were sacrificed 24 hr after the second exposure of each week until the 12-wk study was over. Another 8 mice that completed the 12-wk regimen were immunized with recombinant Hepatitis B surface antigen (HBsAg; three times over an 8-wk period) before sacrifice and analyses of their levels of anti-HBsAg antibody (HBSAb) using ELISA. In all studies, at sacrifice, blood samples were obtained by direct heart puncture and the spleen was removed, weighed and processed for H-E staining and quantitation of CD19 cells. The results indicated that the spleen weight of V2O5-exposed animals peaked at 9 wk (546 +/- 45 vs. 274 +/- 27 mg, p < 0.0001) and thereafter progressively decreased (321 +/- 39 mg at 12 wk, p < 0.001; control spleen = 298 +/- 35 mg). Spleens of V2O5-exposed animals showed an increased number of very large and non-clearly delimited germinal centers (that contained more lymphocytes and megakaryocytes) compared to those of control mice. In addition, their red pulp was poorly delimited and had an increase in CD19+ cells within hyperplasic germinal nodes. The mean HBsAb levels in immunized control mice were greater than that in the exposed hosts (i.e., OD = 0.39 +/- 0.03 vs. 0.11 +/- 0.05, p < 0.01). HBsAb avidity dropped to a value of 40 in V2O5-exposed animals vs. 86 in controls (p < 0.0001). We conclude that the chronic inhalation of V2O5, a frequent particle (PM(2.5)) component, induces histological changes and functional damage to the spleen, each of which appear to result in severe effects on the humoral immune response.

Matrix metalloproteinases 2 and 9 in central nervous system and their modification after vanadium inhalation.

Vanadium (V) derivatives are well-known environmental pollutants and its toxicity has been related with oxidative stress. Toxicity after vanadium inhalation on the substantia nigra, corpus striatum, hippocampus and ependymal epithelium was reported previously. The purpose of this study was to analyse the role of matrix metalloproteinases 2 (MMP-2) and 9 (MMP-9) in the changes observed in brain tissue after chronic V inhalation. Mice were exposed to vaporized, vanadium pentoxide 0.02 m in deionized water for 1 h twice a week, and killed at 1 h, 1, 2 and 4 weeks after exposure. The brain was removed and the olfactory bulb, prefrontal cortex, striatum and hippocampus were dissected and the MMP content was obtained by zymography. The results showed that MMP-9 increased in all the structures at the end of the exposure, although in the hippocampus this increment was evident after 1 week of exposure. When MMP-2 was analysed in the olfactory bulb and prefrontal cortex it remained unchanged throughout the whole exposure, while in the hippocampus it increased at week 4, while in the striatum MMP-2 increased from the second week only, through the whole experiment. These results demonstrate that V increased MMPs in different structures of the CNS and this change might be associated with the previously reported modifications, such as dendritic spine loss and neuronal cell death. The modifications in MMPs could be related with blood-brain barrier (BBB) disruption which was reported previously. Oxidative stress might also be involved in the activation of these gelatinases as part of the different mechanisms which take place in V toxicity in the CNS.

DNA damage as an early biomarker of effect in human health.

In the last few decades the need for new approaches to assess DNA damage has been increasing due to the implications that different insults on genetic material may have on human health. In this context, the identification of how chemical agents with different mechanisms of action (i.e., antineoplastic drugs) damage DNA provides a good model to investigate some cellular and molecular mechanisms underlying the basis of genetic toxicology. The nasal epithelium is the first barrier with which environmental pollutants interact, and for this reason this epithelium can be useful as a sentinel in order to assess the interactions between the environment and the living organisms. Taking these phenomena into account and using a simple, sensitive and rapid method such as the single cell gel electrophoresis, we could obtain information and an initial approach on the DNA status. This assay in combination with other techniques that provide more information about other molecular parameters could give us a better view of the biological status of the living cell.

Nigrostriatal modifications after vanadium inhalation: an immunocytochemical and cytological approach.

Vanadium (V) has increased in the air as a component of suspended particles originated from fuel combustion. In this report, a model of inhaled V in mice was implemented to identify the effect that V has in the corpus striatum and substantia nigra, structures with high concentrations of dopamine and scarce antioxidants burden. Mice inhaled 0.02 M V2O5 1 h twice a week and were sacrificed at points from 1 to 8 weeks after inhalation, perfused, and processed for Golgi method and for tyroxine hidroxylase (TH) inmunocytochemistry. Cytological analysis consisted in counting the number of dendritic spines in 20 medium-size spiny neurons and the number of TH immunoreactive neurons in the substatia nigra pars compacta. Dendritic spine density decreased drastically after V exposure; the same was observed with the TH-positive neurons, which decreased in a time-dependent mode. No previous morphological studies about V and nervous system have been reported. The decrease in spine density and in TH-positive neurons might have functional repercussions that should be studied because the trend of this element in the atmosphere is to increase.

Pulmonary lymphoid lesions in an experimental model of collapsing glomerulopathy in rats.

UNLABELLED: The characterization of lung damage in an experimental model of collapsing glomerulopathy (CG) in rats is described. METHODS: 12 rats were divided into two groups and injected intravenously (iv) with 1 mg/saline in a final volume of 1 ml/ day in the tail vein for 5 days, with fractionated serum from control and CG subjects. Proteinuria was quantified, and the Glomerular filtration rate was calculated based on creatinine clearance (CC). Rats were sacrificed by perfusion fixation at day 5. RESULTS: Rats injected with serum from CG patients developed proteinuria (p<0.001). A decrease in CC (0.68+/-0.19) in these rats was also observed. Glomerular tuft retraction and mesangial proliferation was observed in all rats receiving serum from the CG patients. Peribronchiolar infiltrate integrated mainly by lymphocytes, was identified in all CG rats. In some areas this infiltration disrupted the basement membrane and damaged the epithelium. No histopathological abnormalities in the kidney or lungs were found in rats receiving control serum. CONCLUSION: Patchy pulmonary lymphoid infiltrates were found in the CG model. Up to now there was no information about pulmonary lymphoid infiltration in CG patients. Besides fluid overload due to renal insufficiency or a nephrotic syndrome, other causes of pulmonary involvement in CG patients should be explored.

Genotoxic differences by sex in nasal epithelium and blood leukocytes in subjects residing in a highly polluted area.

We describe differences by sex in genotoxic damage found in a population of medical students exposed to a highly oxidative atmosphere, compared with a control group, measured by the single-cell gel electrophoresis assay and histological changes in nasal epithelium smears. Cells were obtained from the nasal epithelium and blood leukocytes. Higher DNA damage in nasal cells and leukocytes was found in males compared to females and control subjects. The percentage of squamous metaplastic changes in the nasal epithelium was also higher in males compared with females and controls. The co-mutation of normal nasal epithelium by squamous cells might modify its protective function in the nose, increasing the risk of damage to the lower respiratory tract. Although, as medical students, males and females were exposed to the same environment and activity patterns, male genotoxicity damage was higher in control and exposed subjects. More research should be done in order to identify direct or indirect sexual hormone intervention.