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. Author manuscript; available in PMC: 2011 Nov 7.
Published in final edited form as: J Androl. 2008 Dec 18;30(3):325–337. doi: 10.2164/jandrol.108.005934

Table 3.

Damage to seminiferous tubules of C57BL/6 and AKR/N mice after heat treatmenta

Strain Time Post–Heat
Treatment, h
% Tubules With 0–2
Positive Cells/Tubule
% Tubules With 3–5
Positive Cells/Tubule
% Tubules With >5
Positive Cells/Tubule
C57BL/6 8 63.5 ± 5.1 2.2 ± 0.7 35.2 ± 2.8
10 5.0 ± 1.0 13.2 ± 2.5 82.3 ± 2.9
12 0 ± 0 8.2 ± 1.0 91.4 ± 1.2
24 0 ± 0 0 ± 0.02 99.9 ± 0.1
No heat treatment 97.8 ± 1.6 2.2 ± 1.0 0 ± 0.5
AKR/N 8 98.4 ± 1.8 1.4 ± 0.9 0.9 ± 0.1
10 72.2 ± 2.1 5.9 ± 0.3 23.6 ± 3.8
12 35.1 ± 5.3 6.2 ± 2.0 61.1 ± 3.2
24 31.2 ± 6.1 4.3 ± 1.1 62.5 ± 4.6
No heat treatment 99.2 ± 0.08 0.2 ± 0.05 0.6 ± 0.1
a

All genes must have a raw signal no less than 50 in at least 1 strain and 2-fold or more differences in expression between C57BL/6 and the other 2 strains. Tubules with only 0–2 positive cell(s) were considered normal, whereas tubules with more than 5 positive cells were considered damaged. In C57BL/6, damaged tubules increased dramatically at 8 and 10 h after exposure to heat. After 24 h, all tubules showed signs of damage. In contrast, the damage was delayed in AKR/N and even after 24 h, about 30% of the tubules showed no sign of germ cell loss.