Association of melamine exposure with urinary stone and oxidative DNA damage in infants.

There is evidence in experimental animals for the urolithiasis and carcinogenicity of melamine, but no evidence for melamine in humans. To evaluate any association between melamine-contaminated powdered formula (MCPF) feeding and urolithiasis, and further the MCPF feeding and oxidative damage to DNA in infants. A cross-sectional study was carried out to assess urolithiasis and urinary 8-hydroxy-2'-deoxyguanosine (8-OHdG) in four groups of infants according to the type of feeding: (1) Infants receiving over 90% of their intake as MCPF. (2) Infants receiving 50-90% of their intake as MCPF. (3) Infants receiving less than 50% of their intake as MCPF. (4) Infants receiving over 90% of their intake as imported milk powdered formula free of melamine contamination. Groups 1 to 3 are the observation groups, and Group 4 is the reference group. There is a significant correlation between urolithiasis and percentage of MCPF intake. The mean urinary 8-OHdG concentrations for Groups 1, 2, 3, and 4 were: 2.03 +/- 0.52, 1.67 +/- 0.28, 1.90 +/- 0.39, and 1.85 +/- 0.47 micromoles per mole of creatinine, respectively. There were no significant differences in the mean urinary 8-OHdG concentrations among the observation and control groups. There were also no correlation between mean urinary 8-OHdG excretions and percentage of MCPF intake. Our data suggested that melamine exposure were associated with urolithiasis, but it might not cause any increase in oxidative damage of DNA in infants.

Emodin suppresses cell proliferation and fibronectin expression via p38MAPK pathway in rat mesangial cells cultured under high glucose.

Our previous findings demonstrated that emodin could improve the renal function in rats with diabetic nephropathy, but little is known about its molecular mechanisms. In this study, we investigated the effects of emodin on high glucose (HG)-induced cell proliferation and fibronectin (FN) protein expression in rat mesangial cells, and explored the possible mechanism. Cell proliferation and cell cycle were determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and flow cytometry assay, respectively. The protein levels of FN, p-p38MAPK, t-p38MAPK, p-CREB, PPARgamma, and CTGF in rat mesangial cells were detected by Western blot. Our results demonstrated that emodin significantly suppressed HG-induced cell proliferation and arrested cell cycle progress. Protein expression of FN, phospho-p38MAPK, phospho-CREB and CTGF was markedly reduced, and PPARgamma protein level was significantly increased after emodin treatment. In conclusion, emodin suppressed HG-induced cell proliferation and FN expression in rat mesangial cells through inhibiting the p38MAPK pathway involved CREB, PPAPgamma and CTGF, suggesting a potential role of emodin in the treatment of diabetic nephropathy.