Relationships between blood Mg2+ and energy metabolites/enzymes after acute exhaustive swimming exercise in rats.

Magnesium (Mg) plays a central role in neuronal activity, cardiac excitability, neuromuscular transmission, muscular contraction, vasomotor tone, and blood pressure, all of which are significantly related to physical performance. To date, the available data about detection of blood total Mg (tMg; free-ionized, protein-bound, and anion-complex forms) are inconsistent, and there is limited information on blood free-ionized Mg (Mg(2+)) in relation to physical exercise. The aim of this study was to determine the biochemical changes related to energy metabolism after acute exhaustive swimming exercise (AESE) in rats in an attempt to correlate the role of blood Mg(2+) with metabolites/enzymes related to energy production. After AESE, blood Mg(2+), tMg, K(+), partial pressure of carbon dioxide, lactate, total protein (T-PRO), high-density lipoprotein (HDL), creatinine (CRE), blood urea nitrogen (BUN), uric acid (UA), alanine aminotransferase (ALT), aspartate aminotransferase (AST), alanine phosphatase (ALP), lactate dehydrogenase (LDH), and creatinine kinase (CK) were significantly increased, whereas pH, partial pressure of oxygen, oxygen saturation, the Mg(2+)/tMg and Ca(2+)/Mg(2+) ratios, HCO3 (-), glucose, triglyceride (TG), and low-density lipoprotein (LDL) were significantly decreased. During AESE, lactate, T-PRO, albumin, AST, ALP, LDH, CK, CRE, BUN, and UA showed significant positive correlations with changes in blood Mg(2+), while glucose, TG, and LDL correlated to Mg(2+) in a negative manner. In conclusion, AESE induced increases in both blood Mg(2+) and tMg, accompanied by changes in blood metabolites and enzymes related to energy metabolism due to increased metabolic demands and mechanical damages.

Fluoxetine-induced apoptosis in hepatocellular carcinoma cells.

BACKGROUND: In addition to being used to treat mental disorders, a serious complication of cancer, antidepressants have been reported to improve cancer patient immunity, inhibit cell growth and have an antitumor effect on various cancer cell lines. We investigated the apoptotic effect of fluoxetine against the Hep3B human hepatocellular carcinoma cell line. MATERIALS AND METHODS: After treatments of Hep3B cells with fluoxetine, we measured cell viability, reactive oxygen species (ROS), mitochondrial membrane potential (MMP) and activation of mitogen-activated protein kinases (MAPK). RESULTS: Fluoxetine reduced the viability of cancer cells, induced loss of MMP and formation of ROS, reduced expression of extracellular signal-regulated kinase 1/2 and increased expression of c-JUN N-terminal kinase and p38 MAPK. N-Acetylcysteine, an oxidant-scavenger, and 1,2-bis (o-aminophenoxy) ethane-N,N,N',N'-tetraacetic acid (BAPTA-AM), an intracellular Ca(2+) chelator, prevented fluoxetine-induced modulation of MAPK. CONCLUSION: Fluoxetine appears to exhibit an apoptotic effect against Hep3B cells through the loss of MMP, formation of ROS and modulation of MAPK activities.

Korean red ginseng and its primary ginsenosides inhibit ethanol-induced oxidative injury by suppression of the MAPK pathway in TIB-73 cells.

ETHNOPHARMACOLOGICAL RELEVANCE: Panax ginseng (P. ginseng) is one of the most widely used medicinal plants due to its wide spectrum of medicinal effects. Among the currently available Panax ginseng products, Korea red ginseng (KRG) has been shown to exhibit a variety of antioxidative and hepatoprotective action. AIM OF THE STUDY: Our aim was to investigate the effects of KRG and its primary ginsenosides (Rg3 and Rh2) on EtOH-induced injury to mouse hepatocytes (TIB-73). MATERIALS AND METHODS: We investigated the effects of KRG and its primary ginsenoside on EtOH-induced injury to TIB-73 cells and evaluated MAPKs signals as a possible mechanism of action. Hepatocytic injury was evaluated by biochemical assays as cell viability, lactate dehydrogenase (LDH), aspartate aminotransferase (AST), ROS and mitochondria membrane potential (MMP) level in TIB-73 cells. The levels of MAPK activation were analyzed by Western blots. RESULTS: The results showed that exposure of EtOH to TIB-73 cells led to cell death and membrane damage, accompanied by a decrease in cell viability, MMP, and Mg(2+) concentrations, but an increase in LDH, AST, ROS and MAPK activation. KRG and its primary ginsenosides reduced EtOH-induced generation of ROS and the activation of ERK and JNK, and increased Mg(2+) concentrations. CONCLUSION: These results suggest that KRG and its primary ginsenosides inhibit EtOH-induced oxidative injury by suppression of the MAPK pathway in TIB-73 cells.