Human fibroblasts release reactive oxygen species in response to interleukin-1 or tumour necrosis factor-α

TLDR

Human fibroblasts produce reactive oxygen species, mainly superoxide, when stimulated with IL‑1α or TNF‑α. The study found that IL‑1α and TNF‑α trigger a sustained, NAD(P)H‑oxidase–dependent superoxide burst in fibroblasts, producing continuous radical formation, low‑level chemiluminescence, excited carbonyls, and ethane release, with no effect from typical mitochondrial or xanthine oxidase inhibitors.

Abstract

Human fibroblasts in primary culture released reactive oxygen species upon stimulation with cytokines such as interleukin-1 alpha (IL-1) or tumour necrosis factor-alpha (TNF). The primary radical produced was O2.- as determined by e.s.r. spin trapping and cytochrome c reduction. In contrast to the oxidative burst in granulocytes and monocytes, radical formation took place continuously for at least 4 h. Low-level chemiluminescence was increased by stimulation with IL-1 and TNF. Spectral characteristics and tests with azide led to the conclusion that the photoemissive species were excited carbonyls and not singlet oxygen. Further, there was a liberation of ethane from the cells. Radical production and light emission were not altered by either xanthine or allopurinol, nor by azide, cyanide or rotenone. O2.- production increased in the presence of NADH or NADPH, making an NAD(P)H oxidase a likely source.