Quercetin protects HCT116 cells from Dichlorvos-induced oxidative stress and apoptosis.

The present study was designed to assess the possible protective effects of Quercetin (QUER), a flavonoid with well-known pharmacological effects, against Dichlorvos (DDVP)-induced toxicity in vitro using HCT116 cells. The cytotoxicity was monitored by cell viability, reactive oxygen species (ROS) generation, anti-oxidant enzyme activities, malondialdehyde (MDA) production, and DNA fragmentation. The apoptosis was assessed through the measurement of the mitochondrial transmembrane potential (ΔΨm) and caspase activation. The results indicated that pretreatment of HCT116 cells with QUER, 2 h prior to DDVP exposure, significantly decreased the DDVP-induced cell death, inhibited the ROS generation, modulated the activities of catalase (CAT) and superoxide dismutase (SOD), and reduced the MDA level. The reductions in mitochondrial membrane potential, DNA fragmentation, and caspase activation were also attenuated by QUER. These findings suggest that dietary QUER can protect HCT116 cells against DDVP-induced oxidative stress and apoptosis.

Macrophage activation syndrome as the initial manifestation of tumour necrosis factor receptor 1-associated periodic syndrome (TRAPS).

An 11-year-old Turkish girl from a non-consanguineous family was suffering from joint pain, fever, hepatosplenomegaly, and respiratory insufficiency. Laboratory abnormalities were thrombocytopenia, elevated levels of serum transaminases, lactate dehydrogenase, and C-reactive protein (up to 193 mg / l), a hyperferritinaemia of 8030 ng/ml, and an increased sCD25. The tentative diagnosis of macrophage activation syndrome (MAS) was confirmed by the detection of a histiocytosis with haemophagocytosis in the bone marrow. Treatment with dexamethasone, cyclosporine A, and VP16 was successful. However, the diagnosis of MAS on the background of a systemic juvenile idiopathic arthritis was questionable because of recurrent, spontaneously remitting fever phases of 5 to 7 days duration without an obvious infectious aetiology. A positive family history of febrile episodes in three consecutive generations raised the suspicion of a dominantly inherited disease. Genetic studies revealed a likely pathogenetically relevant E56D/p.Glu85Asp mutation in exon 3 of the TNFRSF1A gene. Alterations of the MEFV gene, in contrast, were not found. To our knowledge, this is the first case of a macrophage activation syndrome as the initial manifestation of TRAPS. Similar case reports in patients with the far more common familial Mediterranean fever (FMF) have been published already.