Biosorption experiments for Cr(VI), Cu(II), Cd(II) and Ni(II) were investigated in this study using nonliving biomass of different Pseudomonas species. The applicability of the Langmuir and Freundlich models for the different biosorbent was tested. The coefficient of determination (R 2 ) of both models were mostly greater than 0.9. In case of Ni(II) and Cu(II), their coefficients were found to be close to one. This indicates that both models adequately describe the experimental data of the biosorption of these metals. The maximum adsorption capacity was found to be the highest for Ni followed by Cd(II), Cu(II) and Cr(VI). Whereas the Freundlich constant k in case of Cd(II) was found to be greater than the other metals. Maximum Cr(VI) removal reached around 38% and its removal increased with the increase of Cr(VI) influent. Cu(II) removal was at its maximum value in presence of Cr(VI) as a binary metal, which reached 93% of its influent concentration. Concerning to Cd(II) and Ni(II) similar removal ratios were obtained, since it was ranged between 35 to 88% and their maximum removal were obtained in the case of individual Cd(II) and Ni(II). *Corresponding authorThe presence of heavy metals in aquatic environments is known to cause severe damage to aquatic life, beside the fact that these metals kill microorganisms during biological treatment of wastewater with a consequent delay of the process of water purification. Most of the heavy metal salts are soluble in water and form aqueous solutions and consequently cannot be separated by ordinary physical means of separation.Physico-chemical methods, such as chemical precipitation, chemical oxidation or reduction, electrochemical treatment, evaporative recovery, filtration, ion exchange, and membrane technologies have been widely used to remove heavy metal ions from industrial wastewater. These processes may be ineffective or expensive, especially when the heavy metal ions are in solutions containing in the order of 1-100 mg dissolved heavy metal ions/L (Volesky, 1990a; Volesky, 1990b). Biological methods such as biosorption/ bioaccumulation for the removal of heavy metal ions may provide an attractive alternative to physico-chemical methods (Kapoor and Viraraghavan, 1995).

BackgroundChronic administration of Aluminum is proposed as an environmental factor that may affect several enzymes and other biomolecules related to neurotoxicity and Alzheimer's disease (AD). APE1 a multifunctional protein, functions in DNA repair and plays a key role in cell survival versus cell death upon stimulation with cytotoxic agent, making it an attractive emerging therapeutic target. The promising protective effect of resveratrol (resv), which is known to exert potent anti-inflammatory effects on neurotoxicity induced by aluminum chloride (AlCl3), may be derived from its own antioxidant properties. In the present work we investigated the modulation of APE1 expression during AlCl3-induced neuroinflammation (25 mg/Kg body weight by oral gavages) in experimental rats. We tested the hypothesis that a reactive oxygen species (ROS)-scavenger, resveratrol at 0.5 mg/kg bodyweight, which is known to exert potent anti-inflammatory effects, would attenuate central inflammation and modulate APE1 expression in AlCl3-fed rats. Neuroinflammation-induced genes including β-secretase (BACE), amyloid-β precursor protein (APP), presenilin 2 (PSEN-2) and sirt-2 were determined by RT-PCR. APE1 is determined at mRNA and protein levels and confirmed by immunohistochemistry. The expression of pro-inflammatory cytokines (TNF-α, IL6) and iNOS by the rat brain extract were measured by RT-PCR.ResultOur results indicate that resveratrol may attenuate AlCl3-induced direct neuroinflammation in rats, and its mechanisms are, at least partly, due to maintaining high APE1 level. Resveratrol co-administration with aluminum chloride exerted more protective effect than pre-administration or treatment of induced rats. A significant elevation of APE1 at both mRNA and protein levels was observed in addition to a marked reduction in β-secretase and amyloid-β. We found that AlCl3 stimulated the expression of TNF-α, IL-6, and iNOS in rat brain in which NF-κB was involved. Resveratrol inhibited AlCl3-induced expression and release of TNF-α, IL-6, and iNOS in rat brain.ConclusionsThese findings establish a role for APE1 as a master regulator of AlCl3 dependent inflammatory responses in rat brain. In addition, there was an ameliorative change with resveratrol against AlCl3-induced neurotoxicity. These results suggest that rat brain cells produce pro-inflammatory cytokines in response to AlCl3 in a similar pattern, and further suggest that resveratrol exerts anti-inflammatory effects in rat brain, at least partly, by inhibiting different pro-inflammatory cytokines and key signaling molecules. It might be a potential agent for treatment of neuroinflammation-related diseases, such as AD.

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The levels of arylsulfatases A and B, α-amylase, aspartate transcarbamylase, and γ-glutamyl transpeptidase were investigated during the infection of mice with schistosoma mansoni. This infection caused a significant (p<0.001) increase in the activity of hepatic arylsulfatase B (ASB), aspartate transcarbamylases and γ-glutamyl transpeptidase. A non-significant difference occurred for α-amylase (p<0.3) and arylsulfatase A (p>0.5) when compared to the control. The specific activity of hepatic ASB was progressively increased with the progression of the Schistosoma-infection. Moreover, the kinetic studies of hepatic ASB in Schistosomainfection showed that a slight decrease in the value of K m and about a 40% increase in V max when compared to the control. In addition, the pH optimum of hepatic ASB was altered from 6 to 7 as a result of schistosomiasis. These observations suggest that there are schistosomiasis-associated changes of the catalytic and kinetic properties of hepatic ASB.