Retinol-deficient rats can convert a pharmacological dose of astaxanthin to retinol: antioxidant potential of astaxanthin, lutein, and β-carotene.
Retinol (ROH) and provitamin-A carotenoids are recommended to treat ROH deficiency. Xanthophyll carotenoids, being potent antioxidants, can modulate health disorders. We hypothesize that nonprovitamin-A carotenoids may yield ROH and suppress lipid peroxidation under ROH deficiency. This study aimed to (i) study the possible bioconversion of astaxanthin and lutein to ROH similar to β-carotene and (ii) determine the antioxidant potential of these carotenoids with reference to Na(+)/K(+)-ATPase, antioxidant molecules, and lipid peroxidation (Lpx) induced by ROH deficiency in rats. ROH deficiency was induced in rats (n = 5 per group) by feeding a diet devoid of ROH. Retinol-deficient (RD) rats were gavaged with astaxanthin, lutein, β-carotene, or peanut oil alone (RD group) for 7 days. Results show that the RD group had lowered plasma ROH levels (0.3 µmol/L), whereas ROH rose in astaxanthin and β-carotene groups (4.9 and 5.7 µmol/L, respectively), which was supported by enhanced (69% and 70%) intestinal β-carotene 15,15'-monooxygenase activity. Astaxanthin, lutein, and β-carotene lowered Lpx by 45%, 41%, and 40% (plasma), respectively, and 59%, 64%, and 60% (liver), respectively, compared with the RD group. Lowered Na(+)/K(+)-ATPase and enhanced superoxide dismutase, catalase, and glutathione-S-transferase activities support the lowered Lpx. To conclude, this report confirms that astaxanthin is converted into β-carotene and ROH in ROH-deficient rats, and the antioxidant potential of carotenoids was in the order astaxanthin > lutein > β-carotene.
Department of Biochemistry and Nutrition, Central Food Technological Research Institute, CSIR, Mysore, Karnataka, India.
R K
RK
Sangeetha
V
V
Baskaran
D000818:Animals; D000975:Antioxidants / Q000493:pharmacokinetics / Q000494:pharmacology / Q000627:therapeutic use*; D001711:Biotransformation; D002851:Chromatography, High Pressure Liquid; D004195:Disease Models, Animal; D005227:Fatty Acids / Q000378:metabolism; D015227:Lipid Peroxidation / Q000187:drug effects; D008099:Liver / Q000187:drug effects / Q000201:enzymology / Q000378:metabolism; D014975:Lutein / Q000097:blood / Q000493:pharmacokinetics / Q000494:pharmacology / Q000627:therapeutic use*; D008297:Male; D008862:Microsomes, Liver / Q000187:drug effects / Q000201:enzymology / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism; D014802:Vitamin A Deficiency / Q000188:drug therapy / Q000378:metabolism; D024341:Xanthophylls / Q000097:blood / Q000493:pharmacokinetics / Q000494:pharmacology / Q000627:therapeutic use; D019207:beta Carotene / Q000097:blood / Q000493:pharmacokinetics / Q000494:pharmacology / Q000627:therapeutic use*
D000975:Antioxidants; D005227:Fatty Acids; D024341:Xanthophylls; D019207:beta Carotene; C005948:astaxanthine; D000254:Sodium-Potassium-Exchanging ATPase; D014975:Lutein