Effects of dietary manganese on arterial glycosaminoglycan metabolism in sprague—dawley rats

Abstract

The objectives of this study were to determine whether dietary manganese deficiency alters total glycosaminoglycan (GAG) concentration and composition and glycosyltransferase activity in rat aortas. Sprague-Dawley rats were fed either a manganese-deficient or a manganese-sufficient diet. Arterial GAGs were isolated and quantified by measuring uronic acid content. The individual GAGs were separated and quantified with cellulose acetate electrophoresis. The activity of the enzyme galactosyltransferase I was measured using a 100,000 g particulate fraction and 4-methylumbelliferylxyloside (Xyl-MU) as an acceptor. There was a significant decrease (p < or = 0.05) in uronic acid content in the manganese-deficient (1.18 +/- 0.08 mg/g) rat aortas as compared with the manganese-sufficient (1.59 +/- 0.10 mg/g) ones. Chondroitin sulfate and heparan sulfate concentrations were decreased by 38% (p < or = 0.01) and 36% (p < or = 0.05), respectively, in the manganese-deficient rat aortas. The incorporation of UDP-galactose to acceptors by the manganese-deficient rat aorta preparations was increased by 28% as compared to the manganese-sufficient preparations. These results indicate that manganese is involved in arterial GAG metabolism by affecting the enzyme galactosyltransferase and that changes in GAG concentration and composition with manganese deficiency may ultimately affect arterial wall integrity and subsequently cardiovascular health. This is the first work to demonstrate that manganese nutrition is important in arterial GAG metabolism.

Dietary manganese affects the concentration, composition and sulfation pattern of heparan sulfate glycosaminoglycans in Sprague-Dawley rat aorta

“…The retardation of growth observed in MnD animals was independent of food intake. Retardation of rodent growth in Mn deficiency has also been reported by previous studies (Paynter 1980;Fahim et al 1990;Klimis-Tavantzis et al 1993;Taylor et al 1997) and it seems to be an effect of reduced efficiency of food conversion with dietary Mn depletion (Yang & Klimis-Tavantzis 1998a).…”

“…In the past we reported a decrease in GalAGs concentration of MnD aortas, but the comparison was conducted between MnD and MnS aortas at the time, since 45-50 ppm was used as a control diet group (Yang & Klimis-Tavantzis 1998a, b). Manganese seems to be specifically required for optimal in vivo activity of the enzyme galactosyltransferase I, which participates in the biosynthesis of rat aortic GAGs (Yang & Klimis-Tavantzis 1998a). The increased concentration of GalAG chains in MnS animals might be attributed to an up-regulation of this Mn-dependent enzyme at concentrations of 45-50 ppm.…”

“…The above Mn levels were chosen because studies indicate that a Mn level of less than 1.0 ppm results in Mn deficiency in about fourteen weeks (Klimis-Tavantzis et al 1993;Taylor et al 1997, Yang & Klimis-Tavantzis 1998a. About 10 ppm dietary Mn levels have been reported by the American Institute of Nutrition as an adequate level to prevent deficiency in the rat (Reeves et al 1993).…”

Dietary manganese suppresses α1 adrenergic receptor-mediated vascular contraction

“…Previous studies have shown that Mn may affect blood pressure by decreasing the tension of isolated vascular tissue preparations in vitro [21]. However, there have been no animal studies to 0955 Our laboratory was the first to report that Mn plays an important role in maintaining integrity of blood vessels [22][23][24][25][26]. Manganese is involved in arterial glycosaminoglycan metabolism by affecting the total proteoglycan content of the aorta, altering the molecular weight and sulfation pattern of chondroitin sulfate in the same tissue and thus predisposing the vessel to lipid deposition, lipoprotein oxidation and CVD [24,25].…”

“…However, there have been no animal studies to 0955 Our laboratory was the first to report that Mn plays an important role in maintaining integrity of blood vessels [22][23][24][25][26]. Manganese is involved in arterial glycosaminoglycan metabolism by affecting the total proteoglycan content of the aorta, altering the molecular weight and sulfation pattern of chondroitin sulfate in the same tissue and thus predisposing the vessel to lipid deposition, lipoprotein oxidation and CVD [24,25]. Manganese is essential for preventing surface damage of the aorta and maintaining the density of the extracellular matrix around smooth muscle cells, especially in the medial layer [26].…”