Photocatalytic degradation of Penicillin G in aqueous solutions: Kinetic, degradation pathway, and microbioassays assessment

The photocatalytic degradation of pharmaceutical micropollutants of Penicillin G (PG) was investigated in a photoreactor at a laboratory scale. The impact of type of catalyst, pH, and initial concentration of PG were studied. Maximum removal efficiency was obtained at pH = 6.8, [ZnO]0 = 0.8 g L?1, and [PG]0 = 5 mg L?1 and reaction time of 150 min. The addition of persulfate sodium (PPS) enhanced the efficiency of the photocatalytic reaction. The efficiency of photolysis process in the presence of PPS was significantly improved to 72.72% compared to the classical photocatalysis system (56.71%). Optimum concentration of PPS to completely degraded PG was found to be 500 mg L?1. The QuEChERS extraction, GC-MS/MS method, and concentration technique showed favorable performance identification of the possible mechanism of PG degradation pathway. Toxicity of PG and its by-products were evaluated using microbioassays assessment based on nine selected bacterial strains. Results confirmed the effectiveness of the implemented system and its safe use via the bacteria Bacillus subtilis, which has illustrated significant activity. Due to the high efficiency, facility benefits, and low-cost of the suggested process, the process can be considered for the degradation of various pharmaceutical contaminants in pharmaceutical industry treatment under the optimal conditions.Scopu

Disruption of mitochondrial membrane potential by ferulenol and restoration by propolis extract: Antiapoptotic role of propolis

This paper reports an investigation of the ability of propolis extract (a resinous substance collected by honeybees from various plant sources) to restore the collapse of mitochondrial membrane potential induced by ferulenol, a sesquiterpene prenylated coumarin derivative isolated from the plant Ferula vesceritensis . We show that ferulenol was able to induce the permeability transition pore (PTP) opening. This effect is caused by the interaction of the compound with the mitochondrial respiratory chain, more particularly by the fall of membrane potential and the inhibition of complex II. We have previously demonstrated that this inhibition results from a limitation of electron transfers involved in the respiratory chain and initiated by the reduction of ubiquinone. We hypothesized that the protective effect of propolis could be due to a direct action on mitochondrial functions. So we have investigated in vitro the mitochondrial effects of Algerian propolis using rat liver mitochondria, by analysing their effects on membrane potential, mitochondrial respiration and mitochondrial swelling. We show that propolis extract was able to restore the fall of mitochondrial membrane potential. Taken together these data reveal that propolis extract may be an interesting inhibitor of PTP and provide an additional mechanism by which the natural product propolis extract may restore the mitochondrial membrane potential and to prevent apoptotic process