N acetyl l cysteine nac

JLat 9.2 and TLat 1D5 were diluted to 1 × 10⁶ cells/mL and treated with chemical modulators of latency. PX12, Tiopronin, and Auranofin (redox protein inhibitors) were acquired from Cayman Chemicals. D106 (NSC 155703) was acquired from the National Cancer Institute Developmental Therapeutics Program. PX12 (60 μM), Tiopronin (4 mM), Auranofin (250 nM, 1 μM, or 4 μM), or D106 (10 mM) were added to cells with and without TNF-α (10 ng/mL) for 24 h and analyzed via flow cytometry to determine HIV reactivation. In the case of JLat 9.2, PMA (200 ng/mL) was also used as a latency reversal agent (LRA) to rule out an LRA-specific response to the inhibitors. In MDMs, cells were treated with the same redox protein inhibitors following differentiation and PMA removal from the media (day 0 postdifferentiation). N-acetyl-L-cysteine (NAC; Cayman Chemicals) was added to MLats for 1.5 h before the addition of Auranofin and kept in the media for the duration of treatment (3 h). Cells were analyzed via flow cytometry at different time-points posttreatment.