Despite high plasma levels of vitamin E, red blood cell membranes cont
ain relatively low levels of vitamin E. This suggests the existence of
a selective vitamin E uptake/regeneration system in human red blood c
ell membranes. alpha-Tocopherol binding sites on human red blood cells
are thought to be involved in the uptake of alpha-tocopherol from the
plasma. To understand the role of the uptake system we have compared
the alpha-tocopherol content and binding activity of red blood cells f
rom smokers and non-smokers. The specific binding of [H-3]alpha-tocoph
erol to pure red blood cell preparations from smokers (n = 7, 28.4 +/-
2.8 years) was 30.6 +/- 3.2 fmoles per 3 x 10(8) red blood cells and
for non-smokers (n = 17, 27.9 +/- 1.3 years) was 41.7 +/- 3.7 fmoles p
er 3 x 10(8) red blood cells. Thus alpha-tocopherol uptake activity wa
s significantly lower in smokers (P = 0.05). Red blood cells from smok
ers contained less (1.8 +/- 0.4 mu g/gHb) alpha-tocopherol than non-sm
okers (2.8 +/- 0.3 mu g/gHb), (P < 0.05), despite plasma levels of alp
ha-tocopherol being similar: 12.9 +/- 0.8 mu M in non-smokers vs. 12.7
+/- 0.5 mu M in smokers. However, adjusting plasma alpha-tocopherol f
or total plasma cholesterol plus triacylglycerols showed alpha-tocophe
rol levels were higher (P < 0.01) in non-smokers (2.84 +/- 0.10 mu mol
alpha-tocopherol/mmol [cholesterol+triacylglycerol]) than in smokers
(2.36 +/- 0.11 mu mol alpha-tocopherol/mmol [cholesterol+triacylglycer
ol]). The reduced alpha-tocopherol levels in red blood cells from smok
ers may be due to impairment of alpha-tocopherol uptake activity. The
reduced levels of alpha-tocopherol in smokers red blood cells was not
associated with any changes in cell membrane fluidity. At present it i
s not known whether supplementation of smokers with vitamin E would no
rmalise the alpha-tocopherol uptake activity of red blood cells.