Group | Control | 1 nM | 10 nM | 100 nM | 1 μM | 10 μM | 100 μM |
---|
E1
| 57.4 ± 1.14 | 57.5 ± 1.89 | 57.55 ± 1.78 | 57.37 ± 2.62 | 58.11 ± 1.58 |
60.12 ± 1.12**
|
61.25 ± 1.56***
|
E2
| 57.4 ± 1.14 | 58.00 ± 1.61 | 58.80 ± 1.62 | 58.11 ± 2.11 | 58.40 ± 0.89 |
60.10 ± 1.22**
|
61.81 ± 1.22***
|
E3
| 57.4 ± 1.14 | 56.89 ± 1.75 | 56.14 ± 1.35 | 57.00 ± 1.76 | 57.78 ± 2.45 |
60.22 ± 1.56**
|
61.54 ± 1.67***
|
EE2
| 57.4 ± 1.14 | 57.84 ± 2.09 | 57.70 ± 1.93 | 58.42 ± 1.36 | 58.30 ± 1.98 |
60.10 ± 2.31**
|
61.43 ± 1.37***
|
- Sperm samples from boar E (with no significant responsiveness to E2 at concentration of 1 μM) were capacitated in the presence of six different concentrations (1 nM - 100 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 at 10 μM 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.