Effect of Thyroid Hormones on the Malic Enzyme Activity in Rat Brain during Development

Díez-Guerra, J; Aragón, Marcela; Giménez, Cecilio; Valdivieso, Fernando

doi:10.1159/000112748

Cited by 19 publications

(1 citation statement)

References 11 publications

(12 reference statements)

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“…The modulating effect that the thyroid hormones exert on the central nervous sys tem (CNS) has been revealed on a morpho logical [1,2] and biochemical [3][4][5] level dur ing the functional and structural develop ment of the brain. However, when maturity is reached, the thyroid state exerts a less important effect on the brain [6][7][8].…”

Section: Introductionmentioning

confidence: 99%

Effect of Thyroid Hormones on the Glycolytic Enzyme Activity in Brain Areas of the Rat

Sabell¹,

Morata²,

Quesada³

et al. 1985

Enzyme

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The glycolytic metabolism through the key enzymes, hexokinase, phosphofructokinase, pyruvate kinase and lactate dehydrogenase, have been studied in the brain areas: anterior cortex, amygdala, hypothalamus, septum and hippocampus in adult rats with pharmacologically induced hyperthyroidism. The oxidative metabolism of glucose is accelerated in most brain areas by treatment with high doses of T(3), as is shown by the increase in HK activity, approaching normality on reducing the dose. This decrease can also by observed in the PFK activity through the effect of assayed doses of thyroxine. The anterior cortex is the only brain area that does not show significant variations of PK activity through the effects of treatment with thyroid hormones. On the other hand, a general inhibition of the glycolytic anaerobic pathway by treatment with T(3) was observed.

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Section: Introductionmentioning

confidence: 99%

Effect of Thyroid Hormones on the Glycolytic Enzyme Activity in Brain Areas of the Rat

Sabell¹,

Morata²,

Quesada³

et al. 1985

Enzyme

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A unifying hypothesis of Alzheimer's disease. I. Ageing sets the stage

Heininger

1999

Hum. Psychopharmacol. Clin. Exp.

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In a series of ®ve papers, evidence from neurobiology, endocrinology and immunology is integrated into a holistic, coherent hypothesis accommodating genetic, medical and environmental risk factors into a cascade of pathophysiological events that leads to the clinical manifestation of Alzheimer's disease (AD). The perturbation of the calcium-energy-oxidative stress triangle emerges as pathophysiological leitmotif of ageing and AD. Cellular Ca 2 homeostasis and energy metabolism are closely interdependent. Ca 2 ions regulate the activity of a variety of ratelimiting enzymes of the tricarboxylic acid cycle and respiratory chain. Under physiological circumstances, the supply of energy according to demand is regulated by Ca 2 cycling across mitochondrial membranes. In certain pathological conditions, Ca 2 uncouples electron transfer and oxidative phosphorylation and increases the mitochondrial production of oxygen radicals which in tandem with Ca 2 precipitate the breakdown of mitochondrial function and structure. As most important risk factor, ageing sets the stage for the development of AD. The delicate regulation of the neuroendocrine network which physiologically modulates the Ca 2 -energy-redox homeostasis, deteriorates in ageing, compromising the hormonal balance between neurotrophic/protective and neuroaggressive factors. Thus, levels and/or signal transduction pathways of neurotrophic-factors such as neuropeptide Y, neurotrophins, DHEA/ DHEAS, gonadal hormones, melatonin, insulin, insulin-like growth factors, somatostatin, thyroid hormones, and substance P decay, paralleled by the compromise of the hypothalmic-pituitary-adrenal (HPA)-axis feedback inhibition leading to a hyperresponsiveness to stress and a loss of diurnal rhythm of secretion of neuroaggressive glucocorticoids. Both add up to disrupt Ca 2 and energy homeostasis, put the nerve cells under metabolic and oxidative stress and lead to a compromise of neuronal excitability, signal transduction processes and neuronal plasticity. Subject to the same endocrinological dysregulation, the ageing immune system exhibits a primitive response pattern with impairment of speci®c cellular and activation of unspeci®c humoral and microglial immune responses. Thus, the ageing-related concerted perturbation of the homeostatic control in the neuroendocrinoimmunological network creates phenomena which in many aspects are qualitatively similar to changes in AD and lay the foundations for the development of the disease.

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Clofibrate feeding increases cytoplasmic but not mitochondrial malic enzyme activity in rat kidney cortex

Zelewski

Świerczyński

1989

Cell Biochemistry & Function

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Administration of clofibrate for 21 days to rats increased the malic enzyme activity in the kidney cortex by about 80 per cent. This effect seems to be specific since the drug did not alter significantly the activity either of lactate dehydrogenase, citrate synthase or total mitochondrial protein content in this organ. The increase in activity of malic enzyme in the 13,000 g supernatant (extramitochondrial) fraction in rats treated with the drug was about 80 per cent, whereas in the pellet (mitochondrial fraction) it was about 40 per cent. The specific activity of malic enzyme in the kidney cortex cytosol from clofibrate-treated rats was about twice that in controls. In contrast clofibrate treatment did not affect its specific activity in isolated mitochondria. Calculations showed that 0.57 and 0.53 mumoles min-1 g-1 wet tissue of mitochondrial malic enzyme was obtained in control and clofibrate-treated rats respectively. Thus, clofibrate feeding increases the amount of cytoplasmic but not mitochondrial malic enzyme activity.

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Effect of Thyroid Hormones on the Malic Enzyme Activity in Rat Brain during Development

Cited by 19 publications

References 11 publications

Effect of Thyroid Hormones on the Glycolytic Enzyme Activity in Brain Areas of the Rat

Effect of Thyroid Hormones on the Glycolytic Enzyme Activity in Brain Areas of the Rat

A unifying hypothesis of Alzheimer's disease. I. Ageing sets the stage

Clofibrate feeding increases cytoplasmic but not mitochondrial malic enzyme activity in rat kidney cortex

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