The impact of the invasive species Vespa velutina on honeybees: A new approach based on oxidative stress.

Honeybees have an essential role in ecosystems pollinating wild flowers and cultivated crops, representing an important cultural and economic benefit for humans. Honeybee populations are decreasing over the last decade, due to multifactorial causes. The aim of this field study was to investigate the effects of the presence of the invasive species Vespa velutina, a bee predator, in oxidative stress parameters of honeybee workers. To achieve this objective, positive or negative apiaries for the presence of the V. velutina were selected. Five honeybees from six hives of each apiary were sampled in spring, summer and autumn, analysing a total of 233 samples. Analysis of mRNA expression of oxidative stress-related genes, catalase enzymatic activity and lipid peroxidation were performed. An increase in sod2, tpx3, trxR1, gtpx1, gstS1, coxI, cytC and if2mt genes expression, as well as a raise in catalase activity and lipid peroxidation were observed in V. velutina positive samples. Thus, here we present a new methodology to analyze the impact of the predation pressure of the invasive species V. velutina on honeybees under field conditions. In conclusion, the results obtained in this study indicate the negative impact of the presence of the yellow-legged hornet on honeybees' health and the activation of their antioxidant system to protect them against this biotic stressor. Moreover, the redox status they present could increase the susceptibility of honeybees, essential insects that currently receive many inputs of different stresses, to another stressor.

Proteomic analysis of MCF-7 breast cancer cell line exposed to leptin.

BACKGROUND: Obesity is a well-known factor risk for breast cancer in postmenopausal women. Circulating leptin levels are increased in obese and it has been suggested to play an important role in mammary tumor formation and progression. To contribute to the understanding of the molecular mechanisms underlying leptin action in breast cancer, our aim was to identify proteins regulated by leptin in MCF-7 human breast cancer cells. METHODS: We used two-dimensional gel electrophoresis (2-DE) and matrix assisted laser desorption/ionization time of flight mass spectrometry (MALDI-TOF MS) to identify proteins affected by leptin. RESULTS: Thirty proteins were found differentially expressed in MCF-7 cells after 48 h leptin exposure. Proteins regulated by leptin included proteins previously implicated in breast cancer such as catechol-o-methyltransferase, cathepsin D, hsp27, serine/threonine-protein phosphatase and regulatory proteins of the Ras signaling pathway. Proteins involved in other cellular functions such as stress response, cytosqueleton remodeling and proteins belonging to ubiquitin-proteasome system, were also identified. Furthermore, leptin-treated cells showed a substantial uptake of the serum carrier proteins albumin and alpha-2-HS-glycoprotein. CONCLUSIONS: This screening reveals that leptin influences the levels of key proteins involved in breast cancer which opens new avenues for the study of the molecular mechanisms linking obesity to breast cancer.

17ß-Estradiol regulates oxidative stress in prostate cancer cell lines according to ERalpha/ERbeta ratio.

Estrogen action is mediated by the two receptor isoforms: estrogen receptor alpha and beta. Both receptors are expressed in human prostate tissue and have different action profiles. ERalpha is positively correlated with the malignancy of prostate cancer, while ERbeta may protect against abnormal prostate cell growth. 17ß-Estradiol (E2), at least in part, induces cancerous transformations by causing deleterious mutations through the formation of reactive oxygen species (ROS). The aim was to study the effect of E2 on oxidative stress and the expression of uncoupling proteins (UCPs) and antioxidant enzymes in several prostate cancer cell lines with different ERalpha/ERbeta ratios. The cell prostate lines with a lower ERalpha/ERbeta ratio had lower oxidative stress, which could be partially explained by the increased expression of antioxidant enzymes and UCPs. Moreover, the action of E2 on the expression of antioxidant enzymes and UCPs was dual and dependent on the ERalpha/ERbeta ratio. Treatments with 0.1 nM E2 in cell lines with high ERalpha/ERbeta ratio produced a decrease in antioxidant enzymes and UCPs levels, with an increase in ROS production. These effects disappeared when the treatment was done in the presence of an ERalpha antagonist (MPP). In the cell lines with greatest levels of ERbeta and the lowest ERalpha/ERbeta ratio, E2 treatment caused the up-regulation of antioxidant enzymes and UCPs with a look-up decrease in ROS production. These effects were reversed when the cells were treated with E2 in the presence of an ERbeta antagonist (R,R-THC). On the whole, our results suggest a dual E2 effect; increasing or decreasing oxidative stress in part by modulation of UCPs and antioxidant enzymes according to the abundance ERbeta and ERalpha/ERbeta ratio in prostate cancer cell lines.