The first publications regarding clinical use of
taurine were Italian reports claiming therapeutic efficacy in angina,
intermittent claudication and symptomatic
cerebral arteriosclerosis. A down-regulation of neutrophil activation and endothelial adhesion might plausibly account for these observations. Endothelial
platelet-activating factor (PAF) is a crucial stimulus to neutrophil adhesion and activation, whereas endothelial
nitric oxide (NO) suppresses PAF production and acts in various other ways to antagonize binding and activation of neutrophils.
Hypochlorous acid (HOCl), a neutrophil product which avidly oxidizes many sulfhydryl-dependent
proteins, can be expected to inhibit
NO synthase while up-regulating PAF generation; thus, a vicious circle can be postulated whereby HOCl released by marginating neutrophils acts on capillary or venular endothelium to promote further neutrophil adhesion and activation.
Taurine is the natural detoxicant of HOCl, and thus has the potential to intervene in this vicious circle, promoting a less adhesive endothelium and restraining excessive neutrophil activation. Agents which inhibit the action of PAF on neutrophils, such as
ginkgolides and
pentoxifylline, have documented utility in ischemic disorders and presumably would
complement the efficacy of
taurine in this regard.
Fish oil, which inhibits endothelial expression of various adhesion factors and probably PAF as well, and which suppresses neutrophil
leukotriene production, may likewise be useful in
ischemia. These agents may additionally constitute a non-toxic strategy for treating inflammatory disorders in which activated neutrophils play a prominent pathogenic role. Double-blind studies to confirm the efficacy of
taurine in symptomatic chronic
ischemia are needed.