Key findings
The objectives of this study were: (i) to establish if the flax effect on the liver enzyme gamma-glutamyltranspeptidase is due to the oil or the lignan component; (ii) to assess the flax effect on liver gamma-glutamyltranspeptidase in liver homogenates and in other liver fractions. gGT in liver plays a critical role in the maintenance of intracellular levels of glutathione which is hepatoprotective. In this study, gGT increased in the liver homogenates of flax chow-fed rats, an effect due not to the oil, but lignan, likely secoisolariciresinol diglucoside (SDG), induced and was effected early on, and sustained, after flax exposure. Flax feeding effected an increase in the activity of gGT in isolated plasma membrane fractions which mirrored that in liver homogenates: the same degree of increase was seen in Norlin flax chow-fed and Solin flax chow fed rats. Flax consumption effects an vareXRin the activity of liver gGT which may be linked to hepatoprotection against injury through an increase in reduced glutathione. Flax-induced, SDG-mediated, increase in the activity of the plasma membrane-bound form of liver g-glutamyltranspeptidase may, by increasing GSH, be hepatobeneficial.
ABSTRACT
The effect of 10% flax chow consumption from the 30th to the 130th day after birth was examined in male Fischer 344 rats. The effects of both the high lignan/high oil Norlin strain and a high lignan/low oil Solin strain of flaxseed were compared. Physically and behaviourally there were no differences in rats belonging to the three dietary groups at any time. At 50 and 100 days of dietary exposure, blood glucose levels were the same in Norlin and Solin flax chow-fed and as well as regular chow-fed rats; there were no signs of toxicity in the Norlin and Solin flax-fed rats since their plasma levels of alanine amino transferase were the same and equal to those of regular chow-fed rats. The activity of gamma-glutamyltranspeptidase (gGT) displayed an increase in the liver homogenates of flax chow-fed rats. This increase was the same in Norlin and Solin flax-fed rats at 50 and 100 days. Thus the liver effect was not oil, but lignan, likely secoisolariciresinol diglucoside (SDG), induced and was effected early on, and sustained, after flax exposure. The degree of heat activation of liver homogenate gGT was the same in regular chow-fed and flax chow-fed rats. Compared to liver homogenate gGT activity, the soluble form of gGT was expressed at very low levels while the plasma membrane-bound form of gGT was expressed at very high levels in rat liver in both regular chow-fed and flax chow-fed rats. There was no effect of flax feeding on the soluble form of liver gGT which was expressed at a very low level. Flax feeding effected an increase in the activity of gGT in isolated plasma membrane fractions which mirrored that in liver homogenates: the same degree of increase was seen in Norlin flax chow-fed and Solin flax chow fed rats. Flax consumption effects an increase in the activity of liver gGT at the level of the plasma membrane which is lignan dependent, physiologically relevant and may be linked to hepato protection against injury through an increase in reduced glutathione.
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