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. 2005 Feb;166(2):597–613. doi: 10.1016/s0002-9440(10)62281-x

Table 5.

Functional Analysis of the Endpoint Effects of ETS and Nic on Human Oral KCs

Studied parameters Experimental conditions
Control (no treatment) ETS ETS+αCtxMII Nic Nic+αCtxMII
Cell number (1 × 104/well) 20.4 ± 2.2 24.6 ± 2.4 18.9 ± 2.1 22 ± 2.2 20.8 ± 2.4
Number of TBD+ cells (% of total cells) 3.7 ± 2.1 24.2 ± 4.5* 5.4 ± 2.1 15.3 ± 4.2* 3.1 ± 1.3
Number of TUNEL+ cells (% of total cells) 3.3 ± 1.8 29.1 ± 4.7* 6.9 ± 2.3 21.1 ± 3.7* 4.7 ± 1.2
Number of CK 5+ cells (% of total cells) 79.1 ± 5.7 49.8 ± 4.7* 80.7 ± 5 60.2 ± 4.7* 90.4 ± 6
Number of CK 10+ cells (% of total cells) 11.1 ± 3.7 45.8 ± 4.7* 10.9 ± 4.3 35.3 ± 5* 7.6 ± 3
Caspase 3 activity (RFU) 304 ± 50 1220 ± 78* 634 ± 55 962 ± 36* 512 ± 58
Caspase 8 activity (RFU) 372 ± 63 1413 ± 125* 556 ± 55 1084 ± 87* 484 ± 70

Data shown are means ± SD. 

αCtxMII, α-conotoxin MII; CK, cytokeratin; ETS, environmental tobacco smoke; KCs, keratinocytes; Nic, nicotine; RFU, relative signal; TBD, Trypan Blue dye. 

*

P < 0.05, the rest are P > 0.05, compared to control.