Role of vitamin B6 status on antioxidant defenses, glutathione, and related enzyme activities in
mice with homocysteine-induced oxidative stress
Sammanfattning
Background: Vitamin B6 may directly or indirectly play a role in oxidative stress and the
antioxidant defense system.
Objective: The purpose of this study was to examine the associations of vitamin B6 status with
cysteine, glutathione, and its related enzyme activities in mice with homocysteine-induced oxidative
stress.
Design: Four-week-old male BALB/c mice were weighed and divided into one of four dietary treatment
groups fed either a normal diet (as a control group and a homocysteine group), a vitamin B6-deficient
diet (as a B6-deficient group), or a B6-supplemented diet (a pyridoxine-HCl-free diet supplemented
with 14 mg/kg of pyridoxine-HCl, as a B6 supplement group) for 28 days. Homocysteine thiolactone
was then added to drinking water in three groups for 21 days to induce oxidative stress. At the end of
the study, mice were sacrificed by decapitation and blood and liver samples were obtained.
Results: Mice with vitamin B6-deficient diet had the highest homocysteine concentration in plasma
and liver among groups. Significantly increased hepatic malondialdehyde levels were observed in
the vitamin B6-deficient group. Among homocysteine-treated groups, mice with vitamin B6-deficient
diet had the highest plasma glutathione concentration and relatively lower hepatic glutathione
concentration. The glutathione peroxidase activities remained relatively stable in plasma and liver
whether vitamin B6 was adequate, deficient, or supplemented.
Conclusions: Mice with deficient vitamin B6 intakes had an aggravate effect under homocysteine-
induced oxidative stress. The vitamin B6-deficient status seems to mediate the oxidative stress in
connection with the redistribution of glutathione from liver to plasma, but not further affect
glutathione-related enzyme activities in mice with homocysteine-induced oxidative stress.