Lithium therapy and erythrocyte membrane cation carrier

Naylor, G. J.; Dick, D. A. T.; Dick, E. G.; Moody, J. P.

doi:10.1007/bf00426685

Cited by 54 publications

(26 citation statements)

References 18 publications

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“…In the present study, potentiation with both Li or CBZ exerted a stimulatory effect on the erythrocyte Na,KATPase activity which is consistent with other authors' reports on an increase in this enzyme activity in patients on Li or CBZ [21,32,33]. Increase in ATPase activity correlated significantly with the clinical improvement (decrease in HDRS scores) in the CBZ group.…”

Section: Discussionsupporting

confidence: 81%

Potentiation of Antidepressants with Lithium or Carbamazepine in Treatment-Resistant Depression

1999

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Fifty-nine patients with treatment-resistant depression were randomly allocated an addition of either lithium (Li; 31 patients) or carbamazepine (CBZ; 28 patients) to ongoing antidepressant treatment. The therapeutic efficacy of both strategies, assessed after 28 days, was not significantly different. In the Li group, clinical improvement significantly correlated with decrease in thyroxine concentration. Also, a decrease in cortisol level in Li responders and an increase in nonresponders was observed, suggesting a regulatory effect of Li on the hypothalamic-pituitary-adrenal axis activity. CBZ responders had lower baseline severity of depression than CBZ nonresponders and clinical improvement significantly correlated with increase in erythrocyte ATPase activity in the CBZ group.

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Section: Discussionsupporting

confidence: 81%

Potentiation of Antidepressants with Lithium or Carbamazepine in Treatment-Resistant Depression

1999

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“…In patients taking lithium the in vitro activity of Na+ ,K+-ATPase activity was increased (Naylor et al, 1974) and was significantly higher than in patients not taking lithium (Hokin-Neaverson et al, 1976). Furthermore, there was a correlation between the magnitude of the increase in enzyme activity and the therapeutic response to lithium (Johnston et al, 1980).…”

Section: Discussionmentioning

confidence: 99%

Increase in Na+/K+ pump numbers in vivo in healthy volunteers taking oral lithium carbonate and further upregulation in response to lithium in vitro.

Antia¹,

Wood²,

Aronson³

1992

Brit J Clinical Pharma

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1. We have measured [3H]‐ouabain binding to lymphocyte membranes in eight healthy volunteers before and after they had taken lithium carbonate for 14 days in doses which maintained the serum lithium concentration in the range 0.5‐1.0 mmol 1‐1. 2. There was a statistically significant increase in the [3H]‐ouabain binding capacity of the lymphocyte membranes (reflecting the number of Na+, K+‐ATPase molecules) after 14 days of lithium administration in vivo. This suggests that a failure to increase pump numbers after similar exposure to lithium in vivo in patients with manic‐depressive psychosis is a primary abnormality associated with the disease. 3. In vivo lithium administration did not alter the normal adaptive (upregulatory) response of lymphocyte Na+, K+‐ATPase to standard pharmacological challenges, involving in vitro incubation for 3 days with lithium chloride (8 mmol 1‐1) or sodium ethacrynate (1 mumol 1‐1). 4. We have previously found that there is an impaired response of the Na+, K+‐ ATPase to these in vitro stimuli in patients with manic‐depressive psychosis, and our present data suggest that this abnormality is attributable to the disease itself and not to in vivo lithium therapy. 5. The data also suggest that the increase in vivo Na+/K+ pump activity which we have previously described in healthy volunteers after 21 days of lithium administration is at least partly due to an increase in Na+/K+ pump numbers.

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“…Lithium in manic depressive subjects (but not normal subjects) leads to an increase in erythrocyte Na-K ATPase activity with no change in the number of Na-K ATPase molecules, as estimated by binding of tritiated ouabain (Naylor et al, 1974(Naylor et al, , 1980Glen, 1978). A possible explanation of this effect could be that lithium reduces the inhibitory effect of vanadate on Na-K ATPase.…”

Section: The Effect Of Psychotropic Drugs On Vanadium Metabolismmentioning

confidence: 98%

Vanadium and Manic Depressive Psychosis

Naylor

1984

Nutr Health

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The evidence for the involvement of vanadium in the aetiology of manic depressive psychosis is reviewed. Raised levels of vanadium have been reported in plasma in mania and depression and raised hair levels reported in mania. Lithium has been reported to reduce the inhibition of Na-K ATPase by vanadate. Several groups of psychotropic drugs (e.g. phenothiazines, monoamine oxidase inhibitors) have been shown to catalyse the reduction of vanadate to the less active vanadyl ion. Therapies based on decreasing vanadate levels in the body (e.g. ascorbic acid, EDTA, methylene blue) have been reported to be effective in both depression and mania.

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Lithium therapy and erythrocyte membrane cation carrier

Cited by 54 publications

References 18 publications

Potentiation of Antidepressants with Lithium or Carbamazepine in Treatment-Resistant Depression

Potentiation of Antidepressants with Lithium or Carbamazepine in Treatment-Resistant Depression

Increase in Na+/K+ pump numbers in vivo in healthy volunteers taking oral lithium carbonate and further upregulation in response to lithium in vitro.

Vanadium and Manic Depressive Psychosis

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