Heavy metals in edible specimens around Tagarades landfill after a big fire

The aim of this study was to provide information on the levels of heavy metals (lead and cadmium) in ed­ible specimens around the Tagarades landfill after a big fire.A total of 49 fruit, vegetable and milk samples were collected, according to the Directive 2001/22/EC. The sampling areas were: < 2.5, 2.5, 3, 4, 5, 6, 7, 8, 9 and 10 km around landfill, as well as, 35-40 km away which served as a blank area that was not affected by the landfill. Care was taken to get samples of the same varieties from different selected sites. The samples were wet digested using concentrated nitric and perchloric acid. Cadmium was analyzed using a Flame Atomic Spectrometer and lead an Atomic Absorption Spectrophotometry with graphite furnace atomization. Our results indicate that there was no apparent effect from the landfill fire on lead and cadmium levels found in the tested food samples. These specimens were safe for consumption according to the Draft Commission Regulation on Setting Maximum Limits for Certain Contaminants in Foodstuffs

Heavy metals toxicity

Even though heavy metals are the oldest known toxins harmful to humans, heavy metal toxicity is still a topic that requires further investigation. This paper aims το provid an overview on the most dangerous heavy metals and their negative effects on the human health.Arsenic (As) contaminated underground water and arsenic based agricultural products have generated a worldwide increase of illnesses and deaths that are mainly due to various types of cancer and skin disorders. Industrialization and manufactur­ing made ead (Pb) poisoning a common occurrence, forcing governments to take measures to decrease lead usage. Mercury (Hg), being highly bioaccumulative and with an increasing presence in the environment, when consumed through food is proven to be especially harmful to lactating mothers, fetuses and children. The vast use of admium (Cd) for technological and agricultural purposes poses a high risk of occupational and non-occupational exposure of humans to that element, since it has been confirmed to cause carcinogenesis. Public awareness of the topic is necessary in order to prevent future increase of heavy metal related human diseases and deaths

Alpha2-adrenergic receptors activate cyclic AMP-response element-binding protein through arachidonic acid metabolism and protein kinase A in a subtype-specific manner.

International audienceOn incubation with epinephrine, PC12 cells stably expressing alpha2-adrenergic receptor (alpha2-AR) undergo morphological and biochemical changes characteristic of neuron-like differentiation. The present study shows that alpha2-AR stimulation increases the phosphorylation of the transcription factor cAMP-response element-binding protein (CREB), the activity of a CRE-reporter plasmid and the expression of cyclin D1 with subtype-dependent efficiency (alpha2A approximately alpha2C >> alpha2B). The effects of epinephrine were mimicked by cell exposure to forskolin or to exogenous arachidonic acid (AA) and they were abrogated by prior treatment with the inhibitor of phospholipase C (PLC) (U73122) or the inhibitor of cytochrome P450-dependent epoxygenase, ketoconazole. On the other hand, treatment of the cells with epinephrine caused activation of protein kinase A (PKA), which was fully abolished by ketoconazole. Inhibition of PKA activity with H89 or ketoconazole abolished the effects of epinephrine on CREB, suggesting that activation of the cAMP/PKA pathway by AA epoxy-derivatives is responsible for CREB activation by alpha2-ARs. The effects of epinephrine were unaffected by LY294002. Furthermore, treatment with staurosporine, tyrphostin AG1478, PP1 or PD98059 did not change the extent of CREB phosphorylation but enhanced its transcriptional activity. Altogether, our results demonstrate that, in PC12 cells, the alpha2-AR subtypes cause phosphorylation and activation of CREB through a pathway involving stimulation of PLC, AA release, generation of epoxygenase derivative and increase of PKA activity. They also suggest attenuation of CREB transcriptional activity by mitogen-activated protein kinase, protein kinase C and Src kinases