No abstract

BackgroundSeveral heavy metals have been shown to have toxic effects on the peripheral and central auditory system. Cadmium (Cd2+) is an environmental contaminant showing a variety of adverse effects. Given the current rate of release into the environment, the amount of Cd2+ present in the human body and the incidence of Cd2+-related diseases are expected to increase.ObjectiveThe overall aim of this study was to gain further insights into the mechanism of Cd2+-induced ototoxicity.MethodsCell viability, reactive oxygen species (ROS), mitochondrial membrane potential (MMP), cytochrome c (cyt c), phosphorylated extracellular signal-regulated protein kinase (p-ERK), caspases, morphologic change, and functional changes in HEI-OC1 cells, rat cochlear explants, and mouse cochlea after Cd2+ exposure were measured by flow cytometry, immunohistochemical staining, Western blot analysis, and auditory brainstem response (ABR) recording. Mechanisms underlying Cd2+ototoxicity were studied using inhibitors of different signaling pathways, caspases, and antioxidants.ResultsCd2+ exposure caused cell death, ROS generation, MMP loss, cyt c release, activation of caspases, ERK activation, apoptosis, and finally auditory threshold shift. Cd2+ toxicity interfered with inhibitors of cellular signaling pathways, such as ERK and c-jun N-terminal kinase, and with caspase inhibitors, especially inhibitors of caspase-9 and caspase-3. The antioxidants N-acetyl-l-cysteine and ebselen showed a significant protective effect on the Cd2+ toxicity.ConlcusionsCd2+ is ototoxic with a complex underlying mechanism. However, ROS generation may be the cause of the toxicity, and application of antioxidants can prevent the toxic effect.

Given that tea contains a number of chemical constituents possessing medicinal and pharmacological properties, green tea seed is also believed to contain many biologically active compounds such as saponin, flavonoids, vitamins, and oil materials. However, little is known about the physiologic functions of green tea seed oil. The aim of this study is to investigate the anti-obesity effects of green tea seed oil in C57BL/6J mice and in preadipocyte 3T3L-1 cell lines. In vivo, three groups of mice were fed with a standard diet, a high-fat diet containing 30% shortening, or 30% of green tea seed oil based on a standard diet for 85 days. The levels of total cholesterol, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, triglyceride, glucose, and alanine aminotransferase in blood were analyzed at the end of the study. The mice given green tea seed oil gained less weight compared to mice given the shortening diet (p < 0.01). The plasma level of total cholesterol was decreased by a significant level of 32.4% in mice given the green tea seed oil compared to the mice given the shortening diet (p < 0.01). In addition, 3T3-L1 cells were treated for 2 days to evaluate effects of green tea seed oil on adipocyte differentiation. Green tea seed oil inhibited expression of peroxisome proliferator-activated receptor-gamma(2) and CCAAT/enhancer binding protein-alpha in adipocytes and adipose tissue from the experimental animals. These results indicate that the anti-obesity effects of green tea seed oil might be, in part, through suppression of transcription factors related to adipocyte differentiation.

Lactic acid bacteria are known to exert various physiologic functions in humans. In the current study, we investigated the effects of Soypro, a new soymilk fermented with lactic acid bacteria, like Leuconostoc kimchii, Leuconostoc citreum, and Lactobacillus plantarum, isolated from Kimchi, on adipocyte differentiation in preadipocyte 3T3-L1 cell lines and weight gain or the plasma lipid profile in Sprague-Dawley rats. Adipocyte 3T3-L1 cells treated with Soypro (10 microg/ml) significantly reduced the contents of cellular triglyceride and inhibited cell differentiation by Oil red O staining. Treatment with Soypro (10 microg/ml) for an additional two days in adipocytes inhibited the expression of peroxisome proliferator-activated receptor-gamma2 and CCAAT/enhancer binding protein-alpha, transcription factors of adipocyte differentiation. Based on these in vitro studies, we examined the anti-obesity effect of Soypro in rats for six weeks. Soypro had no significant effect on high-fat diet-induced increases in body weight, food intake, or feed gain ratio. However, the administration of Soypro significantly reduced the concentration of the plasma low density lipoprotein cholesterol. Changes in the plasma levels of total cholesterol and glucose were inclined to decrease in Soypro administrated groups compared with saline treated group. Triglyceride and high density lipoprotein cholesterol values in Soypro fed groups were similar compared to those of saline fed groups. Although further research is needed, these findings suggest that Soypro decreased the levels of low density lipoprotein cholesterol in high-fat diet-induced obesity and might partially inhibit the adipocyte differentiation through the suppression of a transcription factors peroxisome proliferator-activated receptor-gamma2 and CCAAT/enhancer binding protein-alpha.