Endocrine derangement and oxidative stress are two distinguishing features of obesity that have limited the success rate of various management strategies, especially physical activities. The objective of the current study was to examine the effect of 8 weeks of moderate-intensity regular exercise training on oxidative stress, appetite and weight loss in obese women compared with normal-weight women. Sixteen normal-weight (body mass index (BMI) < 25 kg/m 2 ) and fifteen obese women (BMI > 30 kg/m 2 ) exercised on the bicycle ergometer at moderate intensity for 30 min, 3 times per week for 8 weeks. Blood samples were collected at the first day of training and 72 h after the completion of the training program which were then used for the measurement of F2-Isoprostanes, glutathione (GSH), oxidized glutathione (GSSG), leptin, adiponectin and nesfatin-1. Eight (8) weeks of training resulted in lower BMI, insulin, GSSG (P < 0.05), leptin (P < 0.01), and F2-Isoprostanes (P < 0.001) and higher nesfatin-1 levels (P < 0.01) relative to the levels at the pre-test stage in obese women. Also ∆leptin levels after exercise were positively correlated with ∆F2-Isoprostanes and ∆BMI. Eight weeks of moderateintensity regular exercise program did not only induce weight loss and improve oxidative stress, but also modified insulin, leptin and nesfatin-1 concentrations, particularly in obese women.

The current work provides four RNA-based biomarker panel for HCC diagnosis and prognosis.

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We have previously demonstrated that carnitine deficiency aggravated paracetamol-induced hepatopathy and carboplatin-induced nephropathy. As a continuum, we have addressed in the current study as to whether carboplatin-induced myelosuppression would be exacerbated by carnitine deficiency. Challenging male Wistar rats with a single dose of carboplatin (35 mg/kg, IP) induced bone marrow suppression manifested as anemia, leucopenia, thrombocytopenia as well as increased frequencies of the micronucleated bone marrow cells; MPCE and MNCE with notable reduction in the P/N ratio. The platinum drug also elevated serum TNF-a and reduced serum free and total carnitine levels. Besides, ATP levels in red and T cells were lowered. Likewise, the mitochondrial membrane potential in T lymphocytes was reduced following the use of the potentiometric dye; JC-1, and this was well correlated with cellular ATP production. Carnitine deficiency exacerbated carboplatin myelotoxicity as it exaggerated all biochemical, hematological and cytogenetic parameters. To address as to whether carnitine deficiency was a causative clue or merely a sequel of carboplatin myelotoxicity, L-carnitine was supplemented ahead of carboplatin challenege. Herein, L-carnitine mitigated all the biochemical, hematological and cytogenetic effects possibly via modulating the release of TNF-a, cellular ATP production and restoring the mitochondrial membrane potential. Irrespective of the mechanisms involved, the current results may afford the potential role for carnitine supplementation as add-on nutraceutical in carboplatin-based chemotherapy.