The effects of copper deficiency and of chronic overdosage with copper on Border-Leicester and Merino sheep

1948 ◽  
Vol 38 (2) ◽  
pp. 229-241 ◽  
Author(s):  
Hedley R. Marston ◽  
Hector John Lee
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Copper Deficiency ◽  
Myelin Formation ◽  
Merino Sheep ◽  
The Central Nervous System ◽  
Copper Excess

SUMMARYThe effects of copper deficiency and of copper excess on mature Merino and Border-Leicester ewes were studied experimentally over a period of 3½ years with five evenly matched groups of each breed which were all depastured together as one flock on terrain where sheep develop cobalt and copper deficiency. All were treated with the equivalent of 1 mg. Co/day. Copper was administered thrice weekly in doses which provided for individuals of the respective groups the equivalent of nil, 1, 5, 50 and 100 mg. Cu/day.All of the individuals that received only cobalt became anaemic; they lost weight and developed marked symptoms of copper deficiency.The supplement of 1 mg. Cu/day was sufficient to delay the onset of these symptoms, but it failed to increase significantly the concentration of copper in the blood and it was insufficient to ensure normal myelin formation in the central nervous system of lambs born of the ewes which had received this treatment for 2 years prior to mating.

scholarly journals Autonomous requirements of the Menkes disease protein in the nervous system

2015 ◽  
Vol 309 (10) ◽  
pp. C660-C668 ◽  
Author(s):  
Victoria L. Hodgkinson ◽  
Sha Zhu ◽  
Yanfang Wang ◽  
Erik Ladomersky ◽  
Karen Nickelson ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Copper Deficiency ◽  
Copper Homeostasis ◽  
Signs And Symptoms ◽  
Menkes Disease ◽  
Copper Transporter ◽  
Sensorimotor Deficits ◽  
The Central Nervous System

Menkes disease is a fatal neurodegenerative disorder arising from a systemic copper deficiency caused by loss-of-function mutations in a ubiquitously expressed copper transporter, ATP7A. Although this disorder reveals an essential role for copper in the developing human nervous system, the role of ATP7A in the pathogenesis of signs and symptoms in affected patients, including severe mental retardation, ataxia, and excitotoxic seizures, remains unknown. To directly examine the role of ATP7A within the central nervous system, we generated Atp7a Nes mice, in which the Atp7a gene was specifically deleted within neural and glial cell precursors without impairing systemic copper homeostasis, and compared these mice with the mottled brindle ( mo-br) mutant, a murine model of Menkes disease in which Atp7a is defective in all cells. Whereas mo-br mice displayed neurodegeneration, demyelination, and 100% mortality prior to weaning, the Atp7a Nes mice showed none of these phenotypes, exhibiting only mild sensorimotor deficits, increased anxiety, and susceptibility to NMDA-induced seizure. Our results indicate that the pathophysiology of severe neurological signs and symptoms in Menkes disease is the result of copper deficiency within the central nervous system secondary to impaired systemic copper homeostasis and does not arise from an intrinsic lack of ATP7A within the developing brain. Furthermore, the sensorimotor deficits, hypophagia, anxiety, and sensitivity to NMDA-induced seizure in the Atp7a Nes mice reveal unique autonomous requirements for ATP7A in the nervous system. Taken together, these data reveal essential roles for copper acquisition in the central nervous system in early development and suggest novel therapeutic approaches in affected patients.

COPPER DEFICIENCY AND THE CENTRAL NERVOUS SYSTEM

1974 ◽  
Vol 33 (2) ◽  
pp. 226-236 ◽  
Author(s):  
RONALD V. DIPAOLO ◽  
JULIAN N. KANFER ◽  
PAUL M. NEWBERNE
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Copper Deficiency ◽  
The Central Nervous System

Cold-induced inhibition of thermal panting in shorn sheep. 1. Effect of intensity of cold exposure

1973 ◽  
Vol 16 (3) ◽  
pp. 271-283 ◽  
Author(s):  
J. Slee
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Heat Stress ◽  
Respiratory Control ◽  
Specific Inhibition ◽  
Merino Sheep ◽  
Delayed Onset ◽  
Blocking Effects ◽  
The Central Nervous System ◽  
Minimum Intensity

SUMMARYThe delayed onset of heat-induced panting (at 42°C) immediately following previous shearing and exposure to cold was studied in 54 Scottish Blackface and 53 Tasmanian Merino sheep.In control sheep (not previously cold-exposed) thermal panting commenced in 15 min. In cold-treated sheep, when the cold was intensified stepwise from +26°C (+30cC being thermoneutral) down to −10°C, using 2-hr exposures, or lengthened from 2 hr to 16 hr at +8°C, the delay (block) to panting increased non-linearly from 40 to 70 min.The minimum intensity of cold required to produce a block (26°C in Merinos, 22°C in Blackfaces) was similar to that inducing peripheral vasoconstriction. More intense vasoconstriction preceded longer blocks, but vasoconstriction sometimes occurred without a subsequent block.Merinos were more sensitive than Blackfaces to the blocking effects of cold, and, once blocked, the effect in Merinos was less easily removed by re-warming.The time taken for cancellation of the heat debt during heat stress could account for half the block. The remainder, a delay of about 30 min, was attributed to a specific inhibition of respiratory control in the central nervous system.

Copper overload and deficiency both adversely affect the central nervous system of Drosophila

Metallomics ◽  
2014 ◽  
Vol 6 (12) ◽  
pp. 2223-2229 ◽  
Author(s):  
Joab E. C. Hwang ◽  
Marinus de Bruyne ◽  
Coral G. Warr ◽  
Richard Burke
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Copper Deficiency ◽  
The Central Nervous System ◽  
Copper Overload

Ectopic neuronal copper efflux causes a functional copper deficiency leading to developmental lethality in Drosophila.

The biochemistry of copper deficiency - II. Synthetic processes

1956 ◽  
Vol 145 (919) ◽  
pp. 195-205 ◽  
Keyword(s):  
Fatty Acids ◽  
Central Nervous System ◽  
Nervous System ◽  
Nucleic Acid ◽  
Copper Deficiency ◽  
Long Chain Fatty Acids ◽  
Phospholipid Synthesis ◽  
The Central Nervous System ◽  
Long Chain ◽  
Chain Fatty Acids

The biochemistry of copper deficiency is studied in order to gain some understanding of the metabolic disturbances which lead to demyelination of the central nervous system in disease. In the preceding paper we reported our investigation of the enzyme systems, blood chemistry and amino-acid excretion in copper-deficient rats, and in this paper extend the study to investigate the syntheses of phospholipid, long-chain fatty acids, ribose nucleic acid, protein and protohaem. Phospholipid synthesis is found to be depressed considerably in copper deficiency. This is due to a failure in the process of condensation of acyl CoA with α-glycerophosphate to form phosphatidic acids. The reasons are discussed. The syntheses of long-chain fatty acids and ribose nucleic acid are normal, whilst the synthesis of protein is inconstantly affected by copper deficiency. Protohaem synthesis is depressed by a degree which exactly parallels the anaemia. The conclusion is drawn that the anaemia is due to a decrease in haematopoiesis rather than an increased destruction of red cells. The possible interrelationships of the disturbances of phospholipid synthesis and cytochrome oxidase activity and the relevance of each to demyelination of the central nervous system are discussed.

Effects of Hyperoxia on Lung Utrastructure

1970 ◽  
Vol 28 ◽  
pp. 26-27
Author(s):  
Gladys Harrison
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Light Microscopy ◽  
Oxygen Effects ◽  
Age Dependent ◽  
The Central Nervous System ◽  
The Subject ◽  
Space Age ◽  
Alveolar Septa ◽  
Extensive Damage

With the advent of the space age and the need to determine the requirements for a space cabin atmosphere, oxygen effects came into increased importance, even though these effects have been the subject of continuous research for many years. In fact, Priestly initiated oxygen research when in 1775 he published his results of isolating oxygen and described the effects of breathing it on himself and two mice, the only creatures to have had the “privilege” of breathing this “pure air”.Early studies had demonstrated the central nervous system effects at pressures above one atmosphere. Light microscopy revealed extensive damage to the lungs at one atmosphere. These changes which included perivascular and peribronchial edema, focal hemorrhage, rupture of the alveolar septa, and widespread edema, resulted in death of the animal in less than one week. The severity of the symptoms differed between species and was age dependent, with young animals being more resistant.

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