ABSTRACT
Bromate is a byproduct of water disinfection that is produced when waters contain bromide treated with ozone. To investigate the level of the toxicity of bromate and find the most sensitive indicators in a short time, a series of toxicological assessments were conducted including the acute toxicity, cumulative toxicity, genetic toxicity and subacute toxicity of bromate (using Potassium Bromate to represent bromate). The LD50 of orally administered Potassium Bromate was 215 mg/kg in Wistar rats and 464 mg/kg in ICR mice. The cumulative toxicity of Potassium Bromate was not obvious. The Ames test, mouse bone marrow cell micronucleus test and mouse sperm abnormality test did not indicate mutagenicity. The results of the subacute study did not exhibit significant differences in most of the parameters, except the white blood cell count, which was significantly decreased in male rats. In addition, Potassium Bromate influenced the albumin, creatinine, total cholesterol, triglycerides and glucose levels in male rats to various extents. A thorough analysis of the above tests clearly demonstrates that bromate has toxicity, not obvious cumulative toxicity and the white blood cell count can be used as an indicator to reflect the toxicity of bromate and investigate bromate's toxic mechanism.
Subject(s)
Bromates/toxicity , Water Pollutants, Chemical/toxicity , Water Purification , Administration, Oral , Animals , Biomarkers/blood , Body Weight/drug effects , Bromates/administration & dosage , Dose-Response Relationship, Drug , Drinking , Eating/drug effects , Female , Lethal Dose 50 , Leukocytes/drug effects , Male , Mice, Inbred ICR , Micronucleus Tests , Rats, Wistar , Risk Assessment , Spermatozoa/drug effects , Spermatozoa/pathology , Time Factors , Toxicity Tests, Acute/methods , Water Pollutants, Chemical/administration & dosageABSTRACT
Objective:To study the effect of sulforaphane(SFN) on the growth of human bladder cancer cell and its mechanism in vitro. Method:Morphological characteristics of T24 cell nucleus induced by SFN were observed by AO/EB fluorescein staining .The effect of SFN on the T24 cell cycle was determined by flow cytometry. The expression of TrxR at the transcriptional and translational levels were measured by RT-PCR and Western blot methods respectively. Results:(1) After the cells were treated with 10 ?mol/L and 20 ?mol/L SFN for 24 h and 48 h, nuclear fragmentation and apoptotic body were seen under fluorescence microscope. (2) SFN could block the cell cycle at the G0/G1 phase showed by flow cytometry. Moreover, the treatment of 20 ?mol/L SFN for 48h could cause the appearance of sub-G1 before G0/G1 phase. (3) The expression of TrxR mRNA were increased by the treatment of 10 ?mol/L SFN for 4 h, 10 h,24 h ,compared with the control group. Furthermore ,the treatment with high dose SFN (20 ?mol/L ) for 10h or 24 h could induce the expression of TrxR mRNA more significantly . (4)The expression of TrxR protein in the 10 ?mol/L SFN for 24 h group was augmented compared with the control group , and aftertreatment with 20 ?mol/L SFN for 8 h and 24 h, its expression was significantly higher than that in the control group . Conclusion:SFN can inhibit the growth of T24 cell ,induce apoptosis and arrest T24 cell in G0/G1 phase. Its mechanism is associated with the induction of TrxR both at the transcriptional and translational levels.
