Antiglycative and anti-vegf effects of s-ethyl cysteine and s-propyl cysteine in kidney of diabetic mice
Antiglycative and antivascular endothelial growth factor (VEGF) effects of s-ethyl cysteine (SEC), and s-propyl cysteine (SPC) in kidney of diabetic mice were examined. SEC and SPC at 1 and 2 g/L were added to the drinking water for 12 wk. Results showed that diabetic mice with SEC or SPC intake had significantly higher final body weight, lower kidney weight, lower levels of plasma glucose, urinary albumin (UA), and urinary creatinine (UC) (p < 0.05), in which dose-dependent effects were observed in reducing plasma glucose, UA, and UC (p < 0.05). The intake of these compounds significantly and dose-dependently decreased the levels of plasma glycated hemoglobin (HbA1c), renal carboxymethyllysine and urinary glycated albumin (p < 0.05). SEC or SPC intake significantly and dose-dependently diminished renal aldose reductase (AR) activity and enhanced glyoxalase I (GLI) activity (p < 0.05); also significantly decreased renal sorbitol and fructose concentrations (p < 0.05). The intake of SEC or SPC significantly lowered renal VEGF level (p < 0.05), and caused dose-dependent downregulation in AR mRNA expression, and upregulation in GLI mRNA expression (p < 0.05). Our present study suggests the supplement of SEC or SPC might be helpful for the prevention or treatment of diabetic kidney diseases via alleviating renal glycative injury. (Source: Molecular Nutrition)
Selenoprotein deficiency enhances radiation-induced micronuclei formation
The availability of selenium and the levels of specific selenoproteins might affect cancer risk by influencing the ability of DNA damaging agents to cause genomic instability and mutations. Transgenic mice that express reduced levels of selenoproteins and previously shown to be more susceptible to pathology associated with cancer development were used to study this possibility. These mice were exposed to X-rays and DNA damage assessed in the erythrocytes, where micronuclei formation was higher compared to the same cells obtained from irradiated wild-type controls. To determine whether the selenoprotein glutathione peroxidase-1 (GPx-1) might be involved in this protection, its levels were reduced by siRNA targeting in LNCaP human prostate cells. UV-induced micronuclei frequency was higher in these cells compared to control-transfected cells. These results indicate a role for selenoproteins in protecting DNA from damage and support human data implicating GPx-1 as a possible target of the chemoprotective effect of selenium. (Source: Molecular Nutrition)
Metabolism of curcumin and induction of mitotic catastrophe in human cancer cells
In cultured cells, curcumin (CUR) causes cell death by interfering with mitosis and leading to fragmented nuclei and disrupted microtubules, a process named mitotic catastrophe. In order to clarify the role of the known CUR metabolites hexahydro-CUR (HHC) and CUR-glucuronide (CUR-gluc) in mitotic catastrophe, the effects of CUR were studied in three human cancer cell lines with different metabolism of CUR. In Ishikawa and HepG2 cells, CUR was metabolized to HHC and small amounts of octahydro-CUR (OHC), whereas the only metabolism in HT29 cells was the formation of CUR-gluc. Despite their different metabolism, all three cell systems responded to CUR with arrest in G2/M phase and mitotic catastrophe. Fractionation of the cells showed that concentrations of CUR were higher in the ER and cytosol than in the incubation medium by a factor of up to about 150 and 8, respectively. In contrast to CUR, the metabolite HHC and the products of spontaneous degradation did not elicit any effects in Ishikawa cells. These results imply that the causative agent of mitotic catastrophe is the parent CUR molecule, whereas reductive metabolism and chemical degradation render CUR inactive. (Source: Molecular Nutrition)
Selenoprotein deficiency enhances radiation-induced micronuclei formation
The availability of selenium and the levels of specific selenoproteins might affect cancer risk by influencing the ability of DNA damaging agents to cause genomic instability and mutations. Transgenic mice that express reduced levels of selenoproteins and previously shown to be more susceptible to pathology associated with cancer development were used to study this possibility. These mice were exposed to X-rays and DNA damage assessed in the erythrocytes, where micronuclei formation was higher compared to the same cells obtained from irradiated wild-type controls. To determine whether the selenoprotein glutathione peroxidase-1 (GPx-1) might be involved in this protection, its levels were reduced by siRNA targeting in LNCaP human prostate cells. UV-induced micronuclei frequency was higher in these cells compared to control-transfected cells. These results indicate a role for selenoproteins in protecting DNA from damage and support human data implicating GPx-1 as a possible target of the chemoprotective effect of selenium. (Source: Molecular Nutrition)
Metabolism of curcumin and induction of mitotic catastrophe in human cancer cells
In cultured cells, curcumin (CUR) causes cell death by interfering with mitosis and leading to fragmented nuclei and disrupted microtubules, a process named mitotic catastrophe. In order to clarify the role of the known CUR metabolites hexahydro-CUR (HHC) and CUR-glucuronide (CUR-gluc) in mitotic catastrophe, the effects of CUR were studied in three human cancer cell lines with different metabolism of CUR. In Ishikawa and HepG2 cells, CUR was metabolized to HHC and small amounts of octahydro-CUR (OHC), whereas the only metabolism in HT29 cells was the formation of CUR-gluc. Despite their different metabolism, all three cell systems responded to CUR with arrest in G2/M phase and mitotic catastrophe. Fractionation of the cells showed that concentrations of CUR were higher in the ER and cytosol than in the incubation medium by a factor of up to about 150 and 8, respectively. In contrast to CUR, the metabolite HHC and the products of spontaneous degradation did not elicit any effects in Ishikawa cells. These results imply that the causative agent of mitotic catastrophe is the parent CUR molecule, whereas reductive metabolism and chemical degradation render CUR inactive. (Source: Molecular Nutrition)
MedWorm Sponsored Message: Find out how you can get your message across here by sponsoring this MedWorm news feed.