首页 | 本学科首页   官方微博 | 高级检索  
     检索      


Increasing CACNA1C expression in placenta containing high Cd level: an implication of Cd toxicity
Authors:Laorrat Phuapittayalert  Phisid Saenganantakarn  Wisa Supanpaiboon  Supaporn Cheunchoojit  Wiphawi Hipkaeo  Natthiya Sakulsak
Institution:1.Department of Anatomy, Faculty of Medical Science,Naresuan University,Phitsanulok,Thailand;2.Department of Anatomy, School of Medical Science,University of Phayao,Phayao,Thailand;3.Department of Biochemistry, Faculty of Medical Science,Naresuan University,Phitsanulok,Thailand;4.Department of Public Health, Faculty of Science,Buriram Rajabhat University,Buriram,Thailand;5.Department of Anatomy, Faculty of Medicine,Khon Kaen University,Khon Kaen,Thailand
Abstract:Cadmium (Cd) has known to produce many adverse effects on organs including placenta. Many essential transporters are involved in Cd transport pathways such as DMT-1, ZIP as well as L-VDCC. Fourteen pregnant women participated and were divided into two groups: high and low Cd-exposed (H-Cd, L-Cd) groups on the basis of their residential areas, Cd concentrations in the blood (B-Cd), urine (U-Cd), and placenta (P-Cd). The results showed that the B-Cd and U-Cd were significantly increased in H-Cd group (p < 0.05). Interestingly, the P-Cd in H-Cd group was elevated (p < 0.05) and positively related to their B-Cd and U-Cd values (p < 0.05). However, the mean cord blood Cd (C-Cd) concentration in H-Cd group was not significantly increased about 2.5-fold when comparing to L-Cd group. To determine the Cd accumulation in placental tissues, metallothionein-1A (MT-1A) and metallothionein-2A (MT-2A) expressions were used as biomarkers. The results revealed that mean MT-1A and MT-2A mRNAs and MT-1/2 proteins were up-regulated in H-Cd group (p < 0.05). In addition, the Ca channel alpha 1C (CACNA1C) mRNA and protein expressions were noticeably elevated in H-Cd group (p < 0.05). From these findings, we suggested that CACNA1C might be implicated in Cd transport in human placenta.
Keywords:
本文献已被 SpringerLink 等数据库收录!
设为首页 | 免责声明 | 关于勤云 | 加入收藏

Copyright©北京勤云科技发展有限公司  京ICP备09084417号