Stress hormones promote growth of B16-F10 melanoma metastases: an interleukin 6- and glutathione-dependent mechanism

Table 5 ROS generation and the molecular activation of apoptosis upon corticosterone administration to B16-F10 cells with low GSH content

Parameters	Controls	+ Corticosterone	+Corticosterone
			+GSH ester
H₂O₂ (nmol/10⁶ cells)	0.45 ± 0.09	1.74 ± 0.35*	0.73± 0.20*⁺
O₂^.- (ΔFL1)	2.10 ± 0.39	4.33 ± 0.41*	2.65 ± 0.27⁺
mtGSH (nmol/10⁶ cells)	3.2 ± 0.5	1.6 ± 0.4*	6.4 ± 1.0*⁺
MMP (TPM accumulation ration ratio, %)	95 ± 4	52 ± 9	90 ± 7⁺
mtATP (mM)	1.07 ± 0.24	0.66 ± 0.23	0.95 ± 0.18
Cytosolic cytochrome C (% of control)	100 ± 11	165 ± 27	112 ± 15⁺
Caspase 3 (pmol/10⁶ cells x min)	1.36 ± 0.21	3.15 ± 0.77	1.79 ± 0.26⁺

Corticosterone was added as indicated in the caption to Table 1. GSH ester (1 mM) was added 6 h before corticosterone addition. BSO was added to all cells as indicated in the caption to Table 4. Measurements were performed 12 h after corticosterone removal. Data are means + S.D. of 5 or 6 different experiments. *P< 0.01 comparing all conditions versus untreated controls; +P< 0.01 comparing cells treated with corticosterone + GSH ester versus those treated with corticosterone alone.

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