INVESTIGATIVE UROLOGY

Protein oxidation as a novel biomarker of bladder decompensation
Kalorin CM, Mannikarottu A, Neumann P, Leggett R, Weisbrot J, Johnson A, Kogan BA, Levin RM
Albany Medical College, Albany, NY, USA
BJU Int. 2008; 102: 495-9

• Objective: To measure the degree to which partial bladder outlet obstruction (PBOO) results in oxidative bladder damage, which subcellular components of the bladder are affected and whether these changes correlate with bladder function.
• Materials and Methods: In all, 32 rabbits were divided into four groups. Each group underwent PBOO for 1, 2, 4, and 8 weeks, respectively. Bladder tissue from each group was homogenized and separated into subcellular fractions via differential centrifugation. The carbonyl content within the subcellular fractions, including the nuclear, mitochondrial, and microsomal pellets, was then quantified by dot blot analysis.
• Results: Total bladder oxidation increased with duration of obstruction across all subcellular fractions. The largest increase in total oxidation occurred between 4 and 8 weeks. Protein oxidation density in the nuclear and microsomal fractions both showed increases at 2 weeks obstruction, decreases at 4 weeks, and then large increases at 8 weeks. The increase in protein oxidation density between 4 and 8 weeks obstruction was most pronounced in the microsomal fraction.
• Conclusions: Overall bladder protein oxidation increased with the duration of obstruction and increased at a greater rate during the transition to decompensation. Furthermore, the subcellular fraction that exhibited the most oxidation was the microsomal pellet. The amount of protein oxidation correlated with the functional changes in the bladder.
  
  
• Editorial Comment
  In this interesting and welcome experimental study, the authors created surgically partial bladder outlet obstruction (PBOO) in 32 rabbits. They were interested to analyze whether oxidative stress measured after PBOO would correlate with the function of the bladder and whether markers of oxidative stress might serve as a biomarker of the progression to bladder decompensation.
  The authors presented clear evidence that protein oxidation occurs to a significant degree in the PBOO rabbit bladder. They concluded that overall bladder protein oxidation increases with the duration of obstruction and increases at a greater rate during the transition to full decompensation. They speculated that in the clinical setting, the urologist could obtain tissue from the bladder of a patient with BPH and analyze it specifically for microsomal protein oxidation and determine the degree to which the patient is moving towards decompensation. Of course, theoretically, it could be done, but probably it will be hard to put in clinical use.
  The authors are to be congratulated for this elegant study that opens new avenue for the understanding and management of benign prostatic hyperplasia consequences.

Dr. Francisco J. B. Sampaio
Full-Professor and Chair, Urogenital Research Unit
State University of Rio de Janeiro
Rio de Janeiro, RJ, Brazil
E-mail: sampaio@urogenitalresearch.org