Alex Tong-Long Lin1, C H Yang, Kuang-Kuo Chen, Luke S Chang. 1. Department of Surgery, Division of Urology, School of Medicine and Shu-Tien Urological Research Center, National Yang-Ming University, Taipei, Taiwan. lintl@vghtpe.gov.tw
Abstract
OBJECTIVES: Bladder outlet obstruction has shown to damage detrusor mitochondria with impaired detrusor contractility. One likely cause for mitochondrial injury is reactive oxygen species (ROS)-induced damages, including lipid peroxidation injury. We designed this study to examine this hypothesis. MATERIALS AND METHODS: Placing a silicon ring around the bladder neck of male New Zealand rabbits induced bladder outlet obstruction. The bladders were removed 3 (N = 6), 7 (N = 6), and 14 days (N = 8) later. Sham operated animals (N = 6 for each time period) served as the controls. Contractile function of the bladder was assessed by the response of the detrusor strips to bethanechol and field stimulation. Detrusor mitochondrial superoxide dismutase (SOD) activity and mitochondrial content of malondialdehyde (MDA) were determined. Detrusor contents of phosphocreatine and adenine triphosphate (ATP) were assayed. RESULTS: (1) Outlet obstruction induced an increase in the bladder weight and a decrease in the contractile function; (2) mitochondrial SOD activity significantly elevated in every time period of the obstruction, indicating a persistently increased ROS generation; (3) detrusor MDA level increased in 3-day obstruction animals. It returned to the control level in 7- and 14-day groups; (4) phosphocreatine content was significantly reduced in every time period of the obstruction; (5) ATP content was significantly decreased in 3- and 7-day groups; while 14-day obstruction group contained similar level as the sham-operated group. CONCLUSIONS: This study shows that bladder outlet obstruction increases generation of ROS and enhances lipid peroxidation of detrusor mitochondria. The resulted mitochondrial damages might sustain, leading to persistently depressed energy production and impaired detrusor contractility.
OBJECTIVES:Bladder outlet obstruction has shown to damage detrusor mitochondria with impaired detrusor contractility. One likely cause for mitochondrial injury is reactive oxygen species (ROS)-induced damages, including lipid peroxidation injury. We designed this study to examine this hypothesis. MATERIALS AND METHODS: Placing a silicon ring around the bladder neck of male New Zealand rabbits induced bladder outlet obstruction. The bladders were removed 3 (N = 6), 7 (N = 6), and 14 days (N = 8) later. Sham operated animals (N = 6 for each time period) served as the controls. Contractile function of the bladder was assessed by the response of the detrusor strips to bethanechol and field stimulation. Detrusor mitochondrial superoxide dismutase (SOD) activity and mitochondrial content of malondialdehyde (MDA) were determined. Detrusor contents of phosphocreatine and adenine triphosphate (ATP) were assayed. RESULTS: (1) Outlet obstruction induced an increase in the bladder weight and a decrease in the contractile function; (2) mitochondrial SOD activity significantly elevated in every time period of the obstruction, indicating a persistently increased ROS generation; (3) detrusor MDA level increased in 3-day obstruction animals. It returned to the control level in 7- and 14-day groups; (4) phosphocreatine content was significantly reduced in every time period of the obstruction; (5) ATP content was significantly decreased in 3- and 7-day groups; while 14-day obstruction group contained similar level as the sham-operated group. CONCLUSIONS: This study shows that bladder outlet obstruction increases generation of ROS and enhances lipid peroxidation of detrusor mitochondria. The resulted mitochondrial damages might sustain, leading to persistently depressed energy production and impaired detrusor contractility.