A direct correlation between hemoglobin and serum retinol concentrations has been observed (Suharno et al., 1993; Wolde-Gebriel et al., 1993). Anemic rats have been shown to have reduced plasma retinol concentrations when fed a vitamin A-rich diet (Amine et al., 1970), although normal hepatic stores of vitamin A were observed (Staab et al., 1984). Rosales and coworkers (1999) reported that iron deficiency in young rats alters the distribution of vitamin A concentration between plasma and liver. In a cross-sectional study of children in Thailand, serum retinol concentration was positively associated with serum iron and ferritin concentrations (Bloem et al., 1989). Intervention studies among Indonesian girls demonstrated that combining vitamin A with iron supplementation was more effective in increasing hemoglobin concentrations than was giving iron alone (Suharno et al., 1993). As discussed in further detail in Chapter 9, various studies suggest that vitamin A deficiency impairs iron mobilization from stores and therefore vitamin A supplementation improves hemoglobin concentrations (Lynch, 1997).

Zinc is required for protein synthesis, including the hepatic synthesis and secretion of retinol binding protein (RBP) and transthyretin; therefore, zinc deficiency influences the mobilization of vitamin A from the liver and its transport into the circulation (Smith et al., 1974; Terhune and Sandstead, 1972). In animal models, circulating and hepatic concentrations of retinol decline and rise with experimental zinc deficiency and repletion, respectively (Baly et al., 1984; Duncan and Hurley, 1978). In humans, cross-sectional studies and supplementation trials have failed to establish a consistent relationship between zinc and vitamin A status (Christian and West, 1998). Because zinc is important in the biosynthesis of RBP, it has been suggested that zinc intake may positively affect vitamin A status only when individuals are moderately to severely protein-energy deficient (Shingwekar et al., 1979).

Although the alcohol dehydrogenase enzymes involved in the formation of retinal from retinol in the eye are not zinc dependent (Duester, 1996; Persson et al., 1995), zinc-deficient rats had a significant reduction in the synthesis of rhodopsin (Dorea and Olson,