A fluorescence double-quenching study of native lipoproteins in an animal model of manganese deficiency

Abstract

Iodide and acrylamide were applied simultaneously in a double-quenching experiment to compare acrylamide quenching constants for internal and external fluorophores of high-density lipoproteins (HDL1 and HDL2) from manganese-adequate (MnA) and deficient (MnD) rats, free of the electrostatic effects associated with iodide. In MnA HDL1 compared to MnD HDL1, the acrylamide quenching constant for external fluorophores was different (P < 0.1). In MnA HDL2, there were two populations of fluorophores accessible to acrylamide, whereas in MnD HDL2, all fluorophores were accessible to both quenchers. We concluded that there were structural (local environmental) differences, possibly charge-related, around the external fluorophores, and a slightly larger population of buried fluorophores in the MnD HDL1 compared with MnA HDL1. In MnA HDL2, one-third of the fluorophores were accessible to iodide, and all external and internal fluorophores were accessible to acrylamide, whereas in MnD HDL2, all fluorophores were accessible to both quenchers.

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).…”

“…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).…”

“…Diets were mixed in our laboratory from purified ingredients, as described before (Klimis-Tavantzis et al 1993;Taylor et al 1997;Yang & KlimisTavantzis 1998a;Kalea et al 2005). Vitamin (A.O.A.C.…”

“…Manganese also effectively activates sulfotransferases, enzymes involved in GAG sulfation and synthesis (Gundlach & Conrad 1985). We reported in the past that Mn affects arterial glycosaminoglycan (GAG) metabolism by altering the total proteoglycan (PG) concentration, as well as the molecular weight and sulfation pattern of CS in rat aortic tissue (KlimisTavantzis et al 1993;Taylor et al 1997;Yang & Klimis-Tavantzis 1998a, b). Additionally, scanning electron microscopy revealed significantly higher surface damage of the endothelial cell layer in MnD rats and transmission electron microscopy showed less dense extracellular matrix surrounding smooth muscle cells, especially in the medial layers of MnD rats (Ekanayake & Klimis-Tavantzis 1995;Yang & Klimis-Tavantzis 1998a, b).…”

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].…”