1. Rats fed high dietary fructose are documented to form an acquired model of insulin resistance. The present study measured the effects of administration of L-carnitine (CA) on lens protein glycation, oxidative stress and redox homeostasis in rats fed a high-fructose diet. 2. Animals were divided into four groups: (i) an untreated control group (fed starch diet); (ii) an untreated fructose-group (fed a high-fructose diet); (iii) a CA-treated (300 mg/kg per day), fructose-fed group; and (iv) a CA-treated, starch-fed group. After 60 days treatment, lenses were dissected and multiple oxidative stress markers, glycation of proteins and the ratio of oxidized to reduced glutathione (GSSG/GSH) were determined. 3. A significant decline in enzyme and non-enzyme anti-oxidants and an increase in lipid peroxidation products, protein oxidation, protein glycation, GSSG/GSH ratio and aldehyde formation were observed in lens samples obtained from fructose-fed rats. Administration of CA to fructose-fed rats significantly attenuated oxidative damage and protein glycation and returned levels of anti-oxidants to near those seen in the control group. 4. The results of the present study indicate that dietary fructose disturbs lens integrity and exogenous CA may safeguard the lens by preventing glycation and oxidative stress.