Sixteen dogs were allocated to 4 groups in equal number and were fed with Rad ix Rhod od end ri Mollis 0.170, 0.345 and 1.420 g/kg for three months respectively, with one group as control. The results showed that Rad ix Rhod od end ri Mollis can cause focal necrosis, edema, ballooning degeneration and fatty degeneration of liver cells. It can also increase the permeability of glomerulus, and cause edema and even ballooning degeneration of renal tubular epithelial cells. Biochemical analysis showed that GPT and BUN apparently increased. Urine analysis showed that qualitative examination of protein, epithelial cells, white and red blood cells were all positive. It is considered that long-term administration of Rad ix Rhod od end ri Mollis can cause functional and structural damage of liver and kidney, and timely suspension of the drug and treatment may render the damage.

Objective To explore the adverse effect of arsenic trioxide (As2O3) on liver,kidney and heart function during treating children patients with acute promyelocytic leukemia (APL) at therapeutic dose.Methods Sixty-five APL cases received As2O3 by intravenous drip and organic toxicity were selected as our subjects.The indices of liver,heart and kidney were measured.Results Of all subjects,19 cases(29.2％) occurred liver damage,including 15 cases(23.1％) mild and 4 cases(6.2％) moderate toxicity.The levels of alanine aminotransferase of patients before treatment was (19.9 ±9.5) U/L,and (24.3 ± 11.8) U/L,(25.0 ± 14.4) U/L at 1 st and 2nd weeks after treatment,higher than those before the treatment (P ＜ 0.05).However,level of alanine aminotransferase was back to normal at 3th weeks after treatment.Meanwhile the levels of aspartate aminotransferase at 1st,2nd and 3th weeks after treatment were (38.3 ± 16.5),(39.1 ± 15.5),(35.3 ± 20.6) U/L respectively,higher than that before treatment((28.5 ± 8.8) U/L,P ＜ 0.05 or 0.01),and it was back to normal at 4th weeks.(2) The levels of urinary cystatin C were (2.51 ± 1.45) mg/L,(3.05 ± 1.13) mg/L,(2.46 ± 1.21) mg/L at 2nd,3th,4th weeks after treatment,significantly higher than that before treatment ((1.98 ±0.68) mg/L,P ＜0.05 or 0.01).And the levels of urinary β2 microglobulin at 2nd,3th,4th weeks after treatment were significantly higher than that before treatment (P ＜0.05 or 0.01) and back to normal at 5 weeks after treatment.(3) Nine cases at remission stage showed the symptoms of palpitation,precordial discomfort and increased heart rate,and all those symptoms were mild.And the symptoms disappear at the 3th week after the treatment.Creatine kinase at the 2nd weeks after treatment was (90.2 ± 32.5) U/L,higher than that before treatment ((78.5 ± 22.3) U/L).The levels of creatine kinase isoenzyme at 2nd,3th weeks after treatment were (8.3 ± 4.8) U/L,(8.5 ± 5.6) U/L,higher than that before treatment ((6.3 ± 3.5) U/L).The serum creatine kinase mass at 4th weeks((3.9 ±2.0) g/L) was significantly higher than that before treatment ((2.8 ± 1.9) g/L),and then gradually be back to normal.Conclusion The routine dose As2O3 in treatment of APL children show less toxicity in liver,kidney,and heart Those adverse effects are transient,reversible and they occurred at 1-3 week after As2O3 treatment.Serum alanine aminotransferase,aspartate aminotransferase and urinary cystine protease inhibitors,β2 micro ring protein and serum creatine kinase MB mass might be served as sensitive indicators of organ damage.

Objective To analyze differential metabolites (DMs) in the urine of workers with occupational nickel exposure using non-targeted metabolomics, and to screen differential metabolic pathways. Methods A total of 30 nickel exposed workers were selected as the exposure group, and 30 administrative staff from the same factory were selected as the control group using the judgment sampling method. Urine samples of the individuals from the two groups were collected. The ultra-high performance liquid chromatography with quadrupole time-of-flight mass spectrometry and non-targeted metabolomics were used to detect and identify metabolites. The differential metabolic profiles were compared between workers of the two groups, and key differential metabolic pathways and potential biomarkers were screened. The association of DMs and urinary nickel level were evaluated by Spearman correlation coefficients. The sensitivity and specificity of biomarkers were assessed by receiver operating characteristic (ROC) curve analysis. Results A total of 418 metabolites were identified in the urine of worker in the exposure and control groups. The result of principal component analysis and orthogonal partial least squares analysis showed that there were 128 DMs in the urine of workers in the exposure group compared with the control group. These DMs were mainly enriched in glutathione metabolism, carnitine synthesis, and amino acid and nucleotide metabolism pathways, including glycine and serine metabolism. The result of correlation analysis and ROC curve analysis revealed that 4-methylcatechol, 4-vinylphenol sulfate, 2-hydroxyphenylacetone sulfate, 2-dodecylbenzenesulfonic acid, and decylbenzenesulfonic acid could be the potential biomarkers for nickel exposure (all area under the ROC curve >0.800). Conclusion There were significant differences in the urinary metabolic profiles of workers with occupational nickel exposure. The five DMs including 4-methylcatechol, 4-vinylphenol sulfate, 2-hydroxyphenylacetone sulfate, 2-dodecylbenzenesulfonic acid, and decylbenzenesulfonic acid. These DMs could be potential biomarkers of occupational nickel exposure.