The dilemma of hyperoxia following positive pressure mechanical ventilation: role of iron and the benefit of iron chelation with deferasirox.

BACKGROUND AND OBJECTIVE: Increased oxidative stress in patients under treatment with high concentrations of oxygen (hyperoxia) is considered to be one of the major mechanisms of lung injury, which is thought among different mediators, transition metal ion, iron, by generation of very reactive free radicals which play an important role. Disruption of normal iron homeostasis has been reported in hyperoxic conditions. We hypothesized that chelation of iron can reduce hyperoxia-induced lung injury. METHODS: Mechanically ventilated patients, who received oxygen with FiO2 >0.5 for at least 3 days, underwent bronchoscopy before and 72 hours after receiving "Deferasirox". Oxidative injury index and iron homeostasis markers were measured in lavage fluid and plasma. RESULTS: In 12 patients, the concentrations of 8-isoprostane (p=0.005), 8-oxoguanine (p=0.04), carbonyl proteins (p=0.04)--as markers of oxidative stress--decreased significantly in lavage fluid after intervention. Levels of iron-related proteins, ferritin (p=0.04) and transferrin (p=0.005) also decreased significantly in lavage fluid. CONCLUSION: Deferasirox--as an iron chelator--decrease oxidative injury index in hyperoxic condition and it could be consider safe and beneficial agent, along with other supportive measures in hyperoxia-induced lung injury for better toleration of oxygen therapy.

Efficiency of Penicillium chrysogenum PTCC 5037 in reducing low concentration of chromium hexavalent in a chromium electroplating plant wastewater.

The effectiveness of Penicillium chrysogenum was evaluated for reducing Cr(VI) from the wastewater of a chromium electroplating plant. Statistically-based experimental designs were applied to optimize the condition for reducing Cr(VI) to Cr(III). By applying Plackett-Burman factorial design and central composite design as the optimization step, attempts were made to identify optimal values of the three factors that bringing about maximum microorganism activity and therefore maximum hexavalent chromium(VI) bioreduction. It was found that each gram of P. chrysogenum of dry biomass condition could reduce 66 mg of Cr(VI) to Cr(III) in the wastewater of the chromium electroplating plant.

Effects of dopaminergic agents on antinociception in formalin test.

Morphine caused a dose-related antinociception in early phase and late phase of formalin test in mice. The D2 dopamine agonist quinpirole, but not the D1 dopamine agonist SKF 38393, increased the antinociceptive effect of morphine in both phases of the test. The antinociceptive effect of quinpirole also was decreased by sulpiride or domperidone pretreatment in the early phase of test. The D1 antagonist SCH23390, the D2 antagonist sulpiride, or the peripheral D2 dopamine antagonist domperidone, increased the morphine effect. Single administration of SKF38393, quinpirole, SCH23390, sulpiride, and domperidone also induce antinociception. The response of SCH23390, but not that of other dopamine agents, was antagonized with naloxone. The effects of the drugs alone and in combination with morphine have been discussed.

Involvement of cholinergic and opioid receptor mechanisms in nicotine-induced antinociception.

In this work we have studied the influences of nicotinic agents on the antinociception of morphine in formalin test. Nicotine (0.001-0.1 mg/kg) induced antinociception in mice in a dose-dependent manner in the early phase of formalin test, and also potentiated the morphine effect. The nicotinic receptor antagonist, mecamylamine (0.5 mg/kg), but not hexamethonium decreased the antinociception induced by nicotine (0.1 mg/kg) in both phases. The muscarinic receptor antagonist atropine (5 and 10 mg/kg) also decreased the response of nicotine. Mecamylamine, hexamethonium or atropine did not alter morphine antinociceptive response, while naloxone decreased responses induced by nicotine or morphine. The antagonists by themselves did not elicit any response in formalin test, however, high does of mecamylamine tend to increase pain response. It is concluded that central cholinergic and opioid receptor mechanisms may be involved in nicotine-induced antinociception.