Effect of Arbuscular Mycorrhizal Colonization on Cadmium-Mediated Oxidative Stress in Glycine max (L.) Merr.

Cadmium is a heavy metal (HM) that inhibits plant growth and leads to death, causing great losses in yields, especially in Cd hyperaccumulator crops such as Glycine max (L.) Merr. (soybean), a worldwide economically important legume. Furthermore, Cd incorporation into the food chain is a health hazard. Oxidative stress (OS) is a plant response to abiotic and biotic stresses with an intracellular burst of reactive oxygen species (ROS) that causes damage to lipids, proteins, and DNA. The arbuscular mycorrhizal fungal (AMF) association is a plant strategy to cope with HM and to alleviate OS. Our aim was to evaluate the mitigation effects of mycorrhization with AMF Rhizophagus intraradices on soybean growth, nutrients, Cd accumulation, lipid peroxidation, and the activity of different antioxidant agents under Cd (0.7-1.2 mg kg-1 bioavailable Cd) induced OS. Our results suggest that glutathione may act as a signal molecule in a defense response to Cd-induced OS, and mycorrhization may avoid Cd-induced growth inhibition and reduce Cd accumulation in roots. It is discussed that R. intraradices mycorrhization would act as a signal, promoting the generation of a soybean cross tolerance response to Cd pollution, therefore evidencing the potential of this AMF association for bioremediation and encouragement of crop development, particularly because it is an interaction between a worldwide cultivated Cd hyperaccumulator plant and an AMF-HM-accumulator commonly present in soils.

House sparrow biomarkers as lead pollution bioindicators. Evaluation of dose and exposition length on hematological and oxidative stress parameters.

House sparrows (Passer domesticus) have been proposed as a key ecological indicator of urban pollution. Remarkably, we lack knowledge about the physiological effects of lead on this bird species. Therefore, this study was aimed to evaluate the effect of Pb on several physiological parameters in house sparrows exposed to environmental Pb concentrations. In a first experiment, birds were exposed to Pb sub-lethal doses (from 1.3 to 14.0 µg of Pb/g animal/day) during 5 days, which resulted in a dose response increase of blood Pb levels and decrease of blood ALAD activity. However, at the higher doses tested (> 7 µg of Pb/g animal/day) the blood ALAD activity inhibition (~82%) remained constant. Hematocrit and hemoglobin were significantly reduced only at the highest-doses, and the stress indicator, heterophils to lymphocyte (H/L) ratio, did not show apparent changes. In a second experiment, house sparrows were exposed to Pb in drinking water (12.3 ppm) during either 15 or 30 days. Pb concentration used in this study was enough to produce blood lead levels equivalents to those found recently in house sparrows inhabiting urban areas, reduced blood ALAD activity and inversion of the H/L ratio. Decreasing blood ALAD activities were correlated with increasing blood Pb levels. In addition, Pb exposure produced modification in the levels of hepatic antioxidant enzymes, increased GST activity and decreased CAT activity, without lipid peroxidation. In conclusion, our results suggest that blood ALAD activity is a reliable and sensitive biomarker for environmental Pb exposure in house sparrows, additionally chronic exposure produce physiological stress (H/L inversion) and small changes in antioxidant enzyme activity. Finally, this specie could be considered a bioindicator for monitoring the urban Pb contamination.

Cytoprotective mechanisms in rats lung parenchyma with zinc deprivation.

Suboptimal intake of Zinc (Zn) is one of the most common worldwide nutritional problems. The aim of this study is to provide new evidence on the relation between moderate Zn restriction, and cytoprotective functions in airway epithelium. We analyzed the effect of moderate Zn deficiency (ZD) on the expression of several pro and anti-apoptotic proteins and cytoprotective factors (Hsp27 and Hsp 70i), as well as the effect of restoring Zn during the refeeding period. Adult male rats were divided into three groups: Zn-adequate control group, Zn-deficient group and Zn-refed group. Our previous findings showed an important oxidative and nitrosative stress during ZD, this situation is accompanied by inflammation and alterations in the expression of matrix extracellular proteins. We observed a strong immunopositive area of anti and pro-apoptotics proteins in ZD groups. The mRNA levels of Nrf-2, Bax and Bad were increased in ZD, while in ZD refed group its levels were similar to the control values. The increased expression of Nrf-2 is likely to be critical for protection of lung under inflammatory process triggered during ZD. Hsp27 and Hsp 70i showed an increase of immunostaining area but they were not significant. During the supplementation period, heat-shock proteins increased significantly. In conclusion, our results provide further evidence of the pathways involved in cytoprotection and apoptosis caused by ZD. Additional studies are required in order to investigate whether Hsp27 and Hsp70 are consistently associated with cellular stress and inflammation in lung. There may be a beneficial role for improved Zn nutrition or Zn supplements early in lung pathology.

Alterations of the extracellular matrix of lung during zinc deficiency.

Suboptimal intake of Zn is one of the most common nutritional problems worldwide. Previously, we have shown that Zn deficiency (ZD) produces oxidative and nitrosative stress in the lung of rats. We analyse the effect of moderate ZD on the expression of several intermediate filaments of the cytoskeleton, as well as the effect of restoring Zn during the refeeding period. Adult male rats were divided into three groups: Zn-adequate control (CO) group; ZD group; Zn-refeeding group. CerbB-2 and proliferating cell nuclear antigen (PCNA) expression was increased in the ZD group while the other parameters did not change. During the refeeding time, CerbB-2, cytokeratins, vimentin and PCNA immunostaining was higher than that in the CO group. The present findings indicate that the overexpression of some markers could lead to the fibrotic process in the lung. Perhaps ZD implications must be taken into account in health interventions because an inflammation environment is associated with ZD in the lung.

Alteration in the expression of inflammatory parameters as a result of oxidative stress produced by moderate zinc deficiency in rat lung.

Suboptimal intake of dietary zinc (Zn) is one of the most common nutritional problems worldwide. Previously, the authors have shown that zinc deficiency (ZD) produces oxidative and nitrosative stress in lung of male rats. The goal of this study is to test the effect of moderate ZD on insulin-like growth factor (IGF)-1, IGF-binding protein (IGFBP)-5, NADH oxidase (NOX)-2, tumor necrosis factor alpha (TNFalpha), as well as the effect of restoring zinc during the refeeding period. Adult male rats were divided into 3 groups: Zn-adequate control group, Zn-deficient group, and Zn-refeeding group. eNOS, metallothionein (MT) II, and NOX-2 was increased in ZD group. The authors observed an increased gene transcription of superoxide dismutase (SOD)-2 and gluthathione peroxidase (GPx)-1 in ZD group, as well as in ZD-refeeding group, but catalase (CAT) transcription did not change in the treated groups. Proinflammatory factors, such as TNFalpha and vascular cell adhesion molecular (VCAM)-1 increased in ZD, whereas it decreased in ZD refeeding. However, peroxisome proliferator-activated receptor gamma (PPARgamma) and IGF-1 gene transcription decreased in ZD, whereas IGFBP-5 decreased in the ZD group. These parameters are associated to alterations in the lung histoarchitecture. The zinc supplementation period is brief (only 10 days), but it is enough to inhibit some proinflammatory factors. Perhaps, zinc deficiency implications must be taken into account in health interventions because inflammation and prooxidant environment are associated with ZD in lung.