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Quorum sensing (QS) is a major controller of virulence and biofilm formation in pathogenic bacteria. The aim of the research was to screen novel synthetic compounds (18) from 2 series (Pyrazole and Diene dione) for quorum sensing and biofilm inhibitory potential against resistant pathogens isolated from patients with chronic sinusitis. Most of the compounds have documented zone of inhibition against Gram positive strains Staphylococcus aureus , Enterococcus faecalis and moderate activity against Gram negative Klebseilla pneumoniae and Proteus mirabilis in comparison with standard antibiotic. Compounds Q1 and Q7 have given the maximum zone of inhibition 18 and 20 mm with MICs 0.312 mg/mL and .156 mg/mL against S aureus and E faecalis, respectively. Some compounds were equally potent at inhibiting the formation of biofilm which later established by phase contrast microscopy. Regarding quorum sensing inhibition, the tested concentration of synthetic compound UA3 0.313 mg/mL inhibited violacein production without decreasing Chromobacterium pseudoviolaceum count which was significantly lower than determined MIC’s. It was depicted from the results that selected compounds exhibited low level of cytotoxicity toward human red blood cells. Hence, these findings revealed that most novel compounds were effective antibacterial, whereas compound UA3 has shared significant anti-quorum sensing potential against Chromobacterium pseudoviolaceum.

Methotrexate (MTX) is a common chemotherapeutical agent and folate antagonist with reported apoptotic activity in nucleated cells. The presented research work was planned to investigate the eryptotic effects of methotrexate after the exposure of erythrocytes to therapeutical doses (10–15 μM) of methotrexate. Eryptosis and the role of calcium in the stimulation of membrane blebbing were evaluated through the determination of mean cell volume. Oxidative stress induced by methotrexate (10–15 μM) was determined by antioxidative enzyme activities. Cytotoxic activity against human erythrocytes was examined through hemolysis assay. Exposure of erythrocytes to methotrexate results in significant reduction of superoxide dismutase, catalase, and superoxide dismutase activities at 10 and 15 μM in comparison to the untreated cells. Erythrocytes mean cell volume (MCV) was increased after 48 hours exposure of erythrocytes to methotrexate (10 μM). Significantly increased hemolysis percentage was observed at 10 μM after 48 hours incubation of erythrocytes with methotrexate. The results of the study suggested that the therapeutical doses (10–15 μM) of methotrexate may lead to increase in eryptotic and hemolytic activity of erythrocytes through free radical generation and subsequent calcium entry.

Background Bifenthrin is an insecticide and anti-estrogenic compound primarily used to control residential pests by depolarizing sodium gated voltage channels in the nervous system. Eryptosis, the suicidal death of erythrocytes, featured by PS exposure, membrane blebbing and cell shrinkage. Anemia is an outcome of uncontrolled eryptosis. Research Design In this study, erythrocytes were treated with different concentrations (.5-1-1.5 μM) of bifenthrin over a period of 48 hours. In order to investigate the oxidative stress induced by bifenthrin, catalase, superoxide dismutase, and glutathione peroxidase activities were investigated. Results Obtained data indicated the decrease in the enzymes (superoxide dismutase, glutathione peroxidase, and catalase) activities in bifenthrin treated cells at 1 μM concentration. In addition, measurement of cell size and confirmation of the role of calcium in the stimulation of the eryptotic activity of bifenthrin were performed. A significant increase in mean cell volume was found in the presence of bifenthrin and a decrease in mean cell volume in the presence of calcium channel blocker was observed. Similarly, there was also a significant increase in the percentage of hemolysis indicating the necrotic activity of bifenthrin. Conclusions It is concluded that the indicated doses of bifenthrin triggered oxidative stress which may lead to early cell death by eryptosis and hemolysis.

Omeprazole, a proton pump inhibitor blocks the H + /K + -ATPase channels of gastric parietal cells. It is used for the treatment of peptic ulcer. Prolonged use of omeprazole may involve in inducing anemia. The key marker of eryptosis includes membrane blebbing, cell shrinkage and phosphatidylserine (PS) exposure at the cell surface. In current study, the eryptotic, oxidative as well as hemolytic effects of therapeutical doses (0.5, 1 and 1.5 µM) of omeprazole were investigated after exposing erythrocytes for 48 hours. Investigation of eryptosis was done by cell size measurement, PS exposure determination and calcium channel inhibition. As a possible mechanism of omeprazole induced eryptosis, oxidative stress was investigated by determining the catalase, glutathione peroxidase and superoxide dismutase activities. Similarly, necrotic effect of omeprazole on erythrocytes was also evaluated through hemolysis measurement. Results of our study illustrated that 1.5 µM of omeprazole may induce significant decrease in superoxide dismutase, glutathione peroxidase and catalase activities as well as triggered the erythrocytes shrinkage, PS exposure and hemolysis. Role of calcium was also confirmed in inducing erythrocyte shrinkage. It is concluded that the exposure of erythrocytes with 1.5 µM omeprazole may enhance the rate of eryptosis and hemolysis by inducing oxidative stress.

Naproxen sodium is a nonsteroidal anti-inflammatory drug (NSAID) having antipyretic and analgesic properties, mainly used for the treatment of rheumatoid arthritis and osteoarthritis. Eryptosis is an alternative term used for suicidal erythrocyte death. In the current study, eryptotic effect of naproxen sodium characterized by membrane blebbing was investigated in erythrocytes after 48 hours of treatment with different concentrations (1-25 µM). The experimental work related to investigation of eryptosis was done by cell size measurement and confirmation of calcium role in the induction of membrane blebbing. As a possible mechanism of eryptosis, oxidative stress induced by naproxen sodium was determined by catalase, glutathione peroxidase, and superoxide dismutase activities. Similarly, hemolytic effect of naproxen sodium was also determined by hemolysis measurement. Results of our study illustrated that the therapeutic doses (10-25 µM) of naproxen sodium induce oxidative stress, confirmed by significant decrease in superoxide dismutase, catalase, and glutathione peroxidase activities that lead to the triggering of cell death by eryptosis and hemolysis.

Atorvastatin, an inhibitor of 3-hydroxy-3-methylglutaryl-coenzymeA reductase, is usually used for the treatment of hypercholesterolemia. Besides its pharmacological and side actions, its toxic effects on human nucleus devoid of erythrocytes are still unknown. Eryptosis is an alternative term used for suicidal erythrocyte death. Membrane blebbing is among the common markers of eryptosis. In this study, eryptotic effect of atorvastatin was investigated by exposing the erythrocytes for 48 hours to different concentrations (1-10 µM) of atorvastatin. The experimental work related to investigation of eryptosis was done by cell size measurement and calcium channel inhibition. As a possible mechanism of eryptosis, atorvastatin-induced oxidative stress was evaluated by determining catalase, glutathione peroxidase, and superoxide dismutase activities. Similarly, necrotic effect of atorvastatin was also determined by hemolytic assay. Results of our study illustrated that the tested doses of atorvastatin may induce oxidative stress as observed by significant reduction in superoxide dismutase, glutathione peroxidase, and catalase activities as well as induce eryptosis, featured by erythrocytes membrane blebbing. The study concluded that induction of oxidative stress by atorvastatin may lead to eryptosis.