Beschreibung:
<jats:title>Abstract</jats:title><jats:p>In THP‐1 monocytes, cellular proteasome inhibition by ritonavir or ALLN is associated with increased production of oxidative stress. Both compounds produced comparable amounts of oxidative stress; however, normalization by α‐tocopherol occurred solely after inhibition by ritonavir, and not by ALLN. Similar to that, α‐tocopherol could normalize the reduced formation of 3‐nitrotyrosine‐modified proteins only after ritonavir treatment. In the absence of any proteasome inhibitor, intrinsic cellular proteasome activity was not modulated by α‐, β‐, and γ‐tocopherols; however, δ‐tocopherol, α‐tocotrienol, and α‐tocopheryl phosphate could significantly inhibit cellular proteasome activity and increased the level of p27Kip1 and p53. Since oxidative stress was reduced by α‐tocopherol only after proteasome inhibition by ritonavir and not by ALLN, it is concluded that, in this experimental system, α‐tocopherol does not act as an antioxidant but interferes with the inhibitory effect of ritonavir.</jats:p>