Group | Control | 1 nM | 5 nM | 10 nM | 100 nM | 1 μM | 10 μM |
---|
E1
| 55.00 ± 1.56 | 55.5 ± 0.93 | 55.45 ± 1.79 | 56.25 ± 1.28 |
57.60 ± 1.26**
|
59.75 ± 1.58***
|
61.50 ± 0.93***
|
E2
| 55.00 ± 1.56 | 56.00 ± 1.41 |
56.74 ± 1.21*
|
56.80 ± 1.62*
|
57.73 ± 1.27***
|
60.20 ± 1.93***
|
62.00 ± 1.41***
|
E3
| 55.00 ± 1.56 | 54.88 ± 1.36 | 55.14 ± 1.75 | 56.14 ± 1.35 |
57.00 ± 0.89**
|
59.78 ± 1.48***
|
61.71 ± 0.76***
|
EE2
| 55.00 ± 1.56 | 55.44 ± 1.81 | 54.99 ± 2.25 | 55.80 ± 1.93 |
56.82 ± 2.04*
|
58.30 ± 2.91**
|
62.00 ± 1.41***
|
- Sperm samples from boar A (with high responsiveness to E2) were capacitated in the presence of six different concentrations (1 nM - 10 μM) of four estrogens and analyzed by CTC and immunocytochemistry with ACR.2. In each group, at least 5 samples were analyzed. In CTC assay and immunocytochemistry with ACR.2 antibody, only highly correlated results (difference < 5%) were used in the subsequent statistical analysis. All estrogens significantly accelerated the capacitation progress in a concentration-dependent manner. E2 had the first significant effect at 10 nM concentration, other three estrogens at 100 nM concentration. Differences were analyzed by KW-ANOVA; post hoc comparison was performed by multiple comparisons of mean ranks. *P < 0.05, **P < 0.01, ***P < 0.001.