While this shortcoming could be compensated for by dual DNA ubiquitin flow cytometry, we found the current analysis, which was based on the distribution within markers M1-M3, sufficiently informative and reflective of THP exposure.
Because of the previously established association between sperm abnormalities and sperm surface ubiquitination, we expected that a toxic exposure to DNB in the absence of sperm fragmentation (as observed in THP rats) would increase the surface ubiquitination of defective cauda epididymal spermatozoa.
However, there was actually a decrease (see Fig. 4). This could be because of the reduced expression of ubiquitin-conjugating enzymes within the epididymal epithelia and epididymal fluid, among which the reduction in the expression of Ube2d3 was impaired in a highly significant manner (P = 0.003). Accordingly, we have observed the perinuclear accumulation of UBE2, perhaps reflecting the association of UBE2 with the ubiquitin-dependent, endoplasmic reticulum-associated protein-quality control mechanism (ERAD), in the principal cells of the control epithelia (Fig. 9B) but not in the DNB-exposed epithelia.