Table 1.

Oxidative stress and signalling molecules (NF-κB, c-Jun, p53, and caspase-3) are involved in rotenone (ROT)-induced apoptosis in Jurkat T cells.

Treatment/assay	AO/EB/H (%)	PI−/DiOC6(3)+  (%)
Untreated	1 ± 0**	98 ± 1**
ROT (50 μM)	50 ± 3**	51 ± 2**
PDTC (10 nM)	1 ± 0**	97 ± 1**
PDTC (10 nM) + ROT (50 μM)	9 ± 3**	89 ± 3**
PFT (50 nM)	1 ± 0**	98 ± 1**
PFT (50 nM) + ROT (50 μM)	11 ± 2**	87 ± 3**
SP600125 (1 μM)	2 ± 1**	97 ± 1**
SP600125 (1 μM) + ROT (50 μM)	6 ± 2**	93 ± 3**
NSCI (10 μM)	1 ± 0**	98 ± 1**
NSCI (10 μM) + ROT (50 μM)	5 ± 1**	94 ± 2**
NAC (1 mM)	1 ± 0**	98 ± 1**
NAC (1 mM) + ROT (50 μM)	10 ± 3**	89 ± 1**

Jurkat cells (1 × 10⁶ cells/mL) were exposed to ROT (50 μM) in absence or presence of PDTC (10 nM), pifithrin-α (PFT, 50 nM), SP600125 (1 μM) and NSCI (10 μM) signaling inhibitors, and NAC (1 mM) at 37°C for 24 h. Cells were then evaluated for apoptotic nuclei morphology and mitochondrial membrane potential, as described in Material and Methods. The percentage of positive AO/EB/Hoechst staining and PI⁻/DiOC₆(3)⁺ of Jurkat cells treated with or without ROT is expressed as a mean percentage ± S.D. from three independent experiments. **P < 0.001.