Drinking Hydrogen Water Ameliorated Cognitive Impairment in Senescence-Accelerated Mice

Hydrogen has been reported to have neuron protective effects due to its antioxidant properties, but the effects of hydrogen on cognitive impairment due to senescence-related brain alterations and the underlying mechanisms have not been characterized. In this study, we investigated the efficacies of drinking hydrogen water for prevention of spatial memory decline and age-related brain alterations using senescence-accelerated prone mouse 8 (SAMP8), which exhibits early aging syndromes including declining learning ability and memory. However, treatment with hydrogen water for 30 days prevented age-related declines in cognitive ability seen in SAMP8 as assessed by a water maze test and was associated with increased brain serotonin levels and elevated serum antioxidant activity. In addition, drinking hydrogen water for 18 weeks inhibited neurodegeneration in hippocampus, while marked loss of neurons was noted in control, aged brains of mice receiving regular water. On the basis of our results, hydrogen water merits further investigation for possible therapeutic/preventative use for age-related cognitive disorders

Cellular and Molecular Level Mechanisms against Electrochemical Cancer Therapy

Electrochemical treatment (ECT) is a promising new way to induce tumor regression by flowing direct current into the cancer tissue. ECT was applied to different kinds of tumors in clinical studies and showed good results. In addition, basic research has almost not been done in the field of evaluation of efficacy, dose-response, and cytotoxicity. Therefore, the objective is to study the cellular mechanism in the antitumor effect of ECT and to contribute data of basic research of ECT. In the cell-level study, tumor cells (Sarcoma-180, Scc-7, Ehrlich Carcinoma) were studied using ICR mice and C3H mice. In the study group, pH values of control, 10mA × 150secs, 10mA × 300secs, and 10mA × 600secs groups were measured five times each. In histological level studies, ECT was performed on tumors inoculated on the upper part of the right foot of C3H mice. In each group, mice were sacrificed by cervical dislocation 6, 12, and 24 hrs after ECT treatment, and tumors were removed. The excised tumor was fixed in tissue with 10% formalin, and HE staining and apoptosis antibody staining were carried out from the obtained tissue section and observation. In the study at the cellular level, statistically significant differences were observed in all ECT groups in Sarcoma in the tumor growth measurement study compared with the control group. Statistically significant differences were also observed in Scc-7 in all ECT groups compared to the control group. In the intratumoral pH measurement study, there was a statistically significant difference between the anode and the cathode in each group compared to the control group. In the examination at the histological level, microscopic observation of a slide stained with apoptosis antibody with a magnification of 400 times showed that 6hrs after ECT it was stronger and then decreased. By performing ECT, a weak current flows in the living body. As a result, changes in tissue pH, generation of gas, etc. occur. In this study, it was also confirmed that the intratumor pH value becomes strongly acidic on the anode side and strongly alkaline on the cathode side. In addition, this study confirmed the occurrence of gas during treatment of ECT. Changes in the pH and the like cause changes in the environment in the cell, denaturation of proteins, apoptosis, and necrosis. In this study, a significant increase in apoptosis was confirmed in each ECT group compared to the control group. Treatment effects by ECT were also observed in tumor growth measurement studies and tumor weight measurement studies. From these research results, ECT is considered to be effective as a tumor treatment method

A novel GTP-dependent mechanism of ileal muscarinic metabotropic channel desensitization.

1. Cationic current (Icat) was evoked in single isolated smooth muscle cells either by activating muscarinic receptors with the stable muscarinic agonist, carbachol (CCh), or by dialysing cells with GTP-gamma S. It was studied using patch-clamp recording techniques in cells obtained by enzymatic digestion from the longitudinal muscle layer of the guinea-pig small intestine. 2. Icat appears only when muscarinic receptors or G-proteins are activated, but it is strongly voltage-dependent. Its activation could be described by the Boltzmann equation. During desensitization of Icat evoked by 50 microM CCh, the slope factor, k, remained constant whereas the maximal conductance, Gmax, slowly decreased and the potential of half-maximal activation, V1/2, shifted positively by 32 mV during 4 min. 3. At peak response either to extracellular application of CCh (GTP-free, or 1 mM GTP-containing, pipette solution) or to intracellular application of GTP-gamma S (no CCh), the size and voltage-dependent properties of Icat were similar. However, Icat desensitization was slower in the presence of GTP (CCh applied) in the pipette solution and much slower with GTP-gamma S in the pipette (no CCh) compared to GTP-free pipette solution (CCh applied); the decrease in Gmax with time was much delayed and the positive shift of the activation curve was inhibited. GDP-beta S added to the pipette solution at 2 mM abolished Icat in response to applied CCh; 50 microM did not prevent Icat generation but significantly accelerated desensitization. 4. It was concluded that the rate of desensitization of the carbachol-evoked cationic current was due to a decline in the concentration of activated G-protein in the cell, which reduced the maximum number of channels which could be opened and shifted their activation range to less negative potentials