Hypertension / liver oxidative stress / iron chelators



<<snip>>
Iron seems to be an inductor of liver oxidative stress and responsible
for the persistent oxidative stress, most likely through secondary
free-radical release.
<<snip>>

Evolution of liver antioxidant status and iron implication during the
development of deoxycorticosterone-saline hypertension in rats.
Elhaïmeur F, Nicod L, Courderot-Masuyer C, Robin S, Guyon C, Bouhaddi
M, Regnard J, Richert L, Berthelot A
Biol Trace Elem Res. 2005 Dec ; 107(3): 263-76

Hypertension is known to be associated with an oxidative stress
resulting from an imbalance of antioxidant defense mechanisms in
various tissues. The purpose of this study was to investigate the
relationship between the increase of arterial blood pressure, measured
during the gradual development of experimental hypertension in
deoxycorticosterone (DOCA)-salt-treated rats, and an early imbalance of
liver antioxidant status. The levels of liver oxidant/antioxidant
markers and iron were studied during the induction of hypertension in
3-, 6-, and 8-wk DOCA-salt-treated Sprague-Dawley rats. Hepatic
antioxidant defenses were decreased as early as 3 wk of hypertensive
treatment: the decrease of peroxidase-reductase-transferase and
catalase activities was associated with a significant increase of
thiobarbituric acid reactive substances (TBARS) levels. Liver oxidative
stress increased until 6 wk and remained stable at 8 wk of DOCA-salt
treatment. Concurrently, liver iron levels were increased at 6 wk and
returned to normal values after 8 wk of hypertensive treatment. Iron
seems to be an inductor of liver oxidative stress and responsible for
the persistent oxidative stress, most likely through secondary
free-radical release. Thus, our data (1) confirm that hypertension in
DOCA-salt-treated rats might be a free-radical-dependent disease where
hepatic oxidant/antioxidant imbalance is obviously involved from the
beginning of blood pressure elevation and (2) suggest that the use of
suitable iron chelators might reverse liver oxidative stress associated
with the increase of blood pressure.

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Tom


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