Effects of quercetin on oxidative stress biomarkers in methimazole - induced hypothyroid rats.

The objective of the present study was to evaluate the effect of quercetin on oxidative stress biomarkers in methimazole (MMI) - induced hypothyroidism male rats. Hypothyroidism was induced by administering MMI at 20 mg/100 ml in the drinking water, for 1 month. After achieved hypothyroidism, rats received orally 10 or 25 mg/kg of quercetin (QT) for 8 weeks. 60 male wistar rats were randomly divided into 6 groups (group I, control; group II, QT10; group III, QT25; group IV, hypothyroid; group V, hypothyroid+QT10; group VI, hypothyroid+QT25). Liver, kidney and serum TBARS levels significantly increased in hypothyroid rats when compared to controls, along with increased protein carbonyl (PCO) in liver and increased ROS levels in liver and kidney tissues. QT10 and QT25 were effective in decreasing TBARS levels in serum and kidney, PCO levels in liver and ROS generation in liver and kidney. MMI - induced hypothyroidism also increased TBARS levels in cerebral cortex and hippocampus that in turn were decreased in rats treated with QT25. Moreover, the administration of QT25 to hypothyroid rats resulted in decreased SOD activities in liver and whole blood and increased liver CAT activity. Liver and kidney ascorbic acid levels were restored with quercetin supplementation at both concentrations. QT10 and QT25 also significantly increased total oxidative scavenging capacity in liver and kidney tissues from hypothyroid rats. These findings suggest that MMI - induced hypothyroidism increases oxidative stress parameters and quercetin administration could exert beneficial effects against redox imbalance in hypothyroid status.

Alterations in the cholinesterase and adenosine deaminase activities and inflammation biomarker levels in patients with multiple sclerosis.

Multiple sclerosis (MS) is one of the main chronic inflammatory diseases of the CNS that cause functional disability in young adults. It has unknown etiology characterized by the infiltration of lymphocytes and macrophages into the brain. The aim of this study was to evaluate the acetylcholinesterase (AChE) activity in lymphocytes and whole blood, as well as butyrylcholinesterase (BChE) and adenosine deaminase (ADA) activities in serum. We also checked the levels of nucleotides, nucleosides, biomarkers of inflammation such as cytokines (interleukin (IL)-1, IL-6, interferon (IFN)-γ, tumor necrosis factor-alpha (TNF-α) and IL-10) and C-reactive protein (CRP) in serum from 29 patients with the relapsing-remitting form of MS (RRMS) and 29 healthy subjects as the control group. Results showed that AChE in lymphocytes and whole blood as well as BChE, and ADA activities in serum were significantly increased in RRMS patients when compared to the control group (P<0.05). In addition, we observed a decrease in ATP levels and a significant increase in the levels of ADP, AMP, adenosine and inosine in serum from RRMS patients in relation to the healthy subjects (P<0.05). Results also demonstrated an increase in the IFN-γ, TNF-α, IL-1, IL-6 and CRP (P<0.05) and a significant decrease in the IL-10 (P<0.0001) in RRMS patients when compared to control. Our results suggest that alterations in the biomarkers of inflammation and hydrolysis of nucleotides and nucleosides may contribute to the understanding of the neurological dysfunction of RRMS patients.