Liver Mitochondria from Manganese-Deficient and Pallid Mice: Function and Ultrastructure

Hurley, Lucille S.; Theriault, Linda L.; Dreosti, Ivor E.

doi:10.1126/science.170.3964.1316

Cited by 38 publications

(7 citation statements)

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“…A clue was provided by studies involving manganese deficiency and development of the inner ear in rats (HURLEY et al 1960). The congenital ataxia resulting from manganese deficiency (HURLEY, EVERSON and GEIGER 1958;HURLEY and EVERSON 1963) suggested that this trace element might be related to some of the morphogenetic mutations affecting the inner ears of mice (SIDMAN, GREEN and APPEL 1965;DEOL 1968). In a preliminary report, we showed that manganese deficiency in pregnant mice induced a defect of the inner ear which was morphologically and behaviorally indistinguishable from that of pa ( ERWAY, HURLEY and FRASER 1966).…”

mentioning

confidence: 99%

Prevention of Congenital Otolith Defect in Pallid Mutant Mice by Manganese Supplementation

Erway¹,

Fraser²,

Hurley³

1971

Genetics

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confidence: 99%

Prevention of Congenital Otolith Defect in Pallid Mutant Mice by Manganese Supplementation

Erway¹,

Fraser²,

Hurley³

1971

Genetics

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“…Brown adipose tissue and muscle of ob/ob mice have low levels of manganese (Walsh et al 1985), a condition that improves when dietary manganese supplements are provided; low mitochondrial manganese levels result in impaired oxidative capacity (Hurley et al 1970). Thus, high oxidative rates require adequate supplies of manganese and unimpaired absorption/retention.…”

Section: Discussionmentioning

confidence: 99%

Management of dietary essential metals (iron, copper, zinc, chromium and manganese) by Wistar and Zucker obese rats fed a self-selected high-energy diet

et al. 1994

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The balances and content of essential elements (iron, copper, zinc, chromium and manganese) in the body of Wistar, Zucker lean and Zucker obese rats fed a reference or cafeteria diet from day 30 to 60 after birth have been studied. Intestinal iron absorption compensated for low iron content of the cafeteria diet and the extra needs of growth and fat deposition. It can be assumed that the altered energy regulation processes that afflict the genetically obese rat are not directly related to altered iron metabolism. Obese Zucker rats had lower copper tissue concentrations than lean rats, but when fed a cafeteria diet the differences between Zucker rats strains disappear. This cannot be traced to large differences in diet copper concentration. A low diet availability of zinc--such as that of cafeteria-fed fa/fa rats--is easily compensated for by increasing absorption. So, as a consequence, we can conclude that genetic obesity did not impair zinc absorption. There was no deficit of zinc in any of the groups studied; the rats have enough capacity to extract zinc within a wide range of dietary concentrations. The absorption of dietary chromium was inversely proportional to its concentration. The ability to extract chromium from the diet and the very low urinary losses are a consequence of its scarcity in most dietary items. Despite wide variations in the manganese of the diets, the absorption rates were practically unchanged except for obese rats fed the cafeteria diet. It seems that this low absorptive capacity is enough to supply the rat with the manganese it needs, since a sizeable--but subjected to 8-fold-span variations--proportion is lost in the urine. This alone points towards a considerable excess of manganese in both diets studied. Obesity does not have a significant effect on the abilities to absorb and retain minerals, since these processes were more related to dietary availability. Management of essential metals by obese rats depends whether this condition is genetic or induced by diet. Most of the differences observed can be related to differences in diet concentration, to the excess fat content or different metabolic attitude to use substrates of obese animals. The data presented show that the cafeteria diet used adequately serves the mineral needs of the rat, since the rat adapts its absorbing and retaining strategies to match the dietary availability of these minerals.

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“…Any decrease in the cell's ability to maintain adequate steady-state concentrations of these compounds could decrease all UDPlinked substrates for glycosaminoglycan biosynthesis. Ultrastructural abnormalities of mitochondria have been demonstrated by Hurley et al (1970) in the heart, liver, kidney and pancreas of manganesedeficient mice. Oxygen consumption by isolated liver mitochondria from deficient animals is decreased, but the P: 0 ratio is normal (Bell & Hurley, 1973).…”

Section: Discussionmentioning

confidence: 99%

Uridine diphosphate xylosyltransferase activity in cartilage from manganese-deficient chicks

McNatt

Fiser

Elders

et al. 1976

Biochemical Journal

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The glycosaminoglycan content of cartilage is decreased in manganese deficiency in the chick (perosis). The activity of xylosyltransferase, the first enzyme in the biosynthetic pathway of sulphated glycosaminoglycans, was studied in the epiphysial cartilage of 4-week-old chicks which had been maintained since hatching on a manganese-deficient diet. Enzymic activity was measured by the incorporation of [14C]xylose from UDP-[14C]xylose into trichloroacetic acid precipitates. Optimal conditions for the xylosyltransferase assay were established and shown to be the same for both control and manganese-deficient cartilage. Assay of the enzyme by using an exogenous xylose acceptor showed no difference in xylosyltransferase activity between control and manganese-deficient tissue. Further, the extent of xylose incorporation was greater in manganese-deficient than in control cartilage preparations, suggesting an increase in xylose-acceptor sites on the endogenous acceptor protein in the deficient cartilage. 35S turnover in the manganese-deficient cartilage was also increased. The data suggest that the decreased glycosaminoglycan content in manganese-deficient cartilage is due to decreased xylosylation of the acceptor protein plus increased degradation of glycosaminoglycan.

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Liver Mitochondria from Manganese-Deficient and Pallid Mice: Function and Ultrastructure

Cited by 38 publications

References 10 publications

Prevention of Congenital Otolith Defect in Pallid Mutant Mice by Manganese Supplementation

Prevention of Congenital Otolith Defect in Pallid Mutant Mice by Manganese Supplementation

Management of dietary essential metals (iron, copper, zinc, chromium and manganese) by Wistar and Zucker obese rats fed a self-selected high-energy diet

Uridine diphosphate xylosyltransferase activity in cartilage from manganese-deficient chicks

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