Background: Retinol deficiency is a major public health problem world wide, affecting children and women, in particular. It causes a variety of disorders in the body affecting various cellular functions.
Aim of the study: To study the effect of fucoxanthin (FUCO), a non-provitamin-A carotenoid in comparison with retinol (ROH) on changes in antioxidant molecules, lipid peroxidation and membrane bound enzymes in tissue and microsomes, induced by ROH deficiency in rats.
Methods: After induction of ROH deficiency by feeding a diet devoid of ROH for 8 weeks, rats were divided into two groups (n = 20/group) and administered orally a dose of either FUCO (0.83 micromol) or ROH (0.87 micromol). A group of ROH deficient rats (n = 5) and rats (n = 5) fed with ROH sufficient diet was considered as baseline and control groups respectively. Over a period of 8 h, activity of catalase (CAT), glutathione transferase (GST), level of lipid peroxidation (LPx), fatty acids in plasma, liver and liver microsomes and activity of Na(+)K(+)-ATPase in liver microsomes were evaluated.
Results: ROH restriction increased LPx (P < 0.05) in liver (~19%) and plasma (~34%) while the activities of CAT (90 +/- 1%) and GST (17 +/- 4%) decreased compared to control. Significant elevation (91%) was observed for Na(+)K(+)-ATPase activity in liver microsomes of ROH deficient when compared to control group and levels were lowered on administration of ROH (37-69%) and FUCO (51-57%), towards control over a period of 8 h. ROH and FUCO suppressed (P < 0.05) the LPx level (%) in plasma (34-62, 7-85), liver homogenate (9-71, 24-72) and liver microsomes (83-92, 61-87), while the activities of CAT in plasma (89-97%, 91-95%) and liver microsomes (84-93%, 85-93%) and GST in liver homogenate (43-53%, 44-51%) and liver microsomes (36-52%, 22-51%) were increased (P < 0.05) compared to ROH deficient group.
Conclusions: Results show that FUCO, a non-provitamin-A carotenoid protects cell membrane by modulating Na(+)K(+)-ATPase (51-57% lowering) and the activities of CAT and GST at the tissue and microsomal level which are affected by ROH deficiency. This may be due to its antioxidant nature. These in turn reduce LPx caused by ROH deficiency.