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 Cadmium is a toxic and carcinogenic heavy metal that nowadays constitutes a serious environmental health problem. The aim of this study is to review the effects of cadmium on selected inflammatory mediators and markers, such as NF-κB and AP-1 transcription factors, IL-6, TNF-α, IL-1β cytokines, IL-8 or MIP-2 chemokine, MPO, iNOS, MMPs and COX-2 enzymes, PGE2 (product of COX-2 enzyme), ICAM-1, VCAM-1 and PECAM-1 adhesion molecules, and CRP. The research strategy identified articles; available in , published between 1998 and 2012; we included both in vivo and in vitro studies carried out on humans and rodents. Most of the reviewed research findings suggest that cadmium in micromolar concentrations (especially in the 1-10 μM range) causes up-regulation of the mediators and markers of inflammation, and appears to have pro-inflammatory properties. However, it is worth mentioning that a contradictory or even opposite hypothesis exists, which suggests cadmium to be an anti-inflammatory factor. Further research including detailed histological analyses should solve this discrepancy. Nevertheless, it appears that the main reason for these contradictory findings is the experimental setup: different biological systems analyzed and different doses of cadmium applied.
Vanadium belongs to the group of transition metals and is present in the air and soil contaminants in large urban agglomerations due to combustion of fossil fuels. It forms numerous inorganic compounds (vanadyl sulfate, sodium metavanadate, sodium orthovanadate, vanadium pentoxide) as well as complexes with organic compounds (BMOV, BEOV, METVAN). Depending on the research model, vanadium compounds exhibit antitumor or carcinogenic properties. Vanadium compounds generate ROS as a result of Fenton's reaction or of the reaction with atmospheric oxygen. They inactivate the Cdc25B2 phosphatase and lead to degradation of Cdc25C, which induces G2/M phase arrest. In cells, vanadium compounds activate numerous signaling pathways and transcription factors, including PI3K-PKB/Akt-mTOR, NF-κB, MEK1/2-ERK, that cause cell survival or increased expression and release of VEGF. Vanadium compounds inhibit p53-dependent apoptosis and promote entry into the S phase of cells containing functional p53 protein. In addition, vanadium compounds, in particular organic derivatives, have insulin-mimetic and antidiabetic properties. Vanadium compounds lower blood glucose levels in animals and in clinical trials. They also inhibit the activity of protein tyrosine phosphatase 1B. By activating the PI3K-PKB/Akt pathway, vanadium compaunds increase the cellular uptake of glucose by the GLUT4 transporter. The PKB/Akt pathway is also used to inactivate glycogen synthase kinase-3. The impact of vanadium compounds on inflammatory reactions has not been fully studied. Vanadium pentoxide causes expression of COX-2 and the release of proinflammatory cytokines in a human lung fibroblast model. Other vanadium compounds activate NF-κB in macrophages by activating IKKβ.
Although many countries now have programs to lower the levels of lead in the environment, human exposure to Pb remains of concern to public health officials worldwide. The mechanisms of lead toxicity are still not fully understood, but recent findings have recognized the significance of the lead-induced impairment of the cell energy metabolism. This review outlines recent hypotheses and evidence on the role of nucleotide purines in erythrocyte metabolism regulation. It also describes the resynthesis and decomposition of purine nucleotides in erythrocytes, lead distribution in blood and its influence on purine conversion pathways and both glycolytic and pentosophosphate pathway enzymes in erythrocytes.
For the purpose of this work an epiphytic lichen species, Hypogymnia physodes (L.)Nyl., was used. Thalli of the lichen were treated with solutions of nitrate salts of heavy metals, including Zn(NO3)(2), Cu(NO3)(2), Pb(NO3)(2), and Cd(NO3)(2). To simulate the acid rain impact, pH of the metal mixture was lowered to pH 4, using Na2S2O5. Content of heavy metals was determined after a standard UV mineralization method (water solution) and burning method (in temperature 450 degreesC- thalli), using a Microcomputer Voltage-ammeter Analyser (MAW). After two months exposure of the lichen to the mixture of heavy metal nitrates it was ascertained that there was an increase of accumulation of Zn, Pb, Cu, and Cd in the thalli; a decrease of thalli pH caused increased uptake of toxic elements by the lichen; Pb and Cd remained mainly on the surface of the thalli and in the cell walls, whilst Zn and Cu penetrated to the protoplast.
One of the major functions of magnesium is the maintenance of proper electric potential of neurons. Pathological conditions associated with systemic magnesium deficiencies may be associated with disturbance of numerous neurophysiological processes. These may include neuron function, transmission of nerve impulses, neuromuscular transmission, muscle contraction and vasomotor reflex. Therefore, magnesium deficiencies, particularly those associated with hypomagnesemia, are a source of problems for neurologists. Migraine is one of the most common neurological disorders. Despite many years of research, pathophysiology of migraine has not been elucidated. The predominant opinion is that the onset of migraine headaches is associated with cerebral vascular spasms. Based on the available knowledge of biological functions of magnesium, at least several feasible mechanisms for prevention or reduction of the intensity of migraine attacks by magnesium ions have been proposed. The goal of this review is to summarize the literature reports on magnesium in the pathogenesis of migraine and to identify the potential uses for magnesium compounds in prevention and treatment of migraine headaches.
In the present experiments the effect of perinatal lead exposure on development of morphine dependence in rats was examined. Female rats were gavaged daily with 0.1 % lead acetate solution. Lead ions were administered through pregnancy and two months through lactation. In the same time control animals received water. The development of morphine dependence was obtained by administration of increasing doses (10, 20, 30, 40, 50, 50 mg/kg, ip) of morphine for six consecutive days in lead intoxicated rats and in control animals. 20 min after the last injection of morphine the withdrawal signs were induced by application of naloxon at dose of 2 mg/kg, ip. Secondly, the development of morphine tolerance to antinociception activity was studied in the tail-flick test in lead intoxicated rats. Then rats received morphine (10 mg/kg, ip) for seven consecutive days and test was performed on 1st and 7th day of the experiment. The experiments have shown that in lead intoxicated rats morphine withdrawal signs (jumping, wet dog shakes) were significantly potentiated than in control animals. The morphine tolerance was also more expressed in lead intoxicate rats. The obtained results have shown that prenatal lead exposure intensify the effects of chronic treatment with morphine in rats.
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