16
Views
0
CrossRef citations to date
0
Altmetric
Research Article

HYPOTHALAMIC DIGOXIN, CEREBRAL CHEMICAL DOMINANCE, AND PATHOGENESIS OF PULMONARY DISEASES

&
Pages 235-258 | Published online: 07 Jul 2009
 

Abstract

The isoprenoid pathway is a key regulatory pathway in the cell. It synthesizes digoxin, an endogenous membrane Na+-K+ ATPase inhibitor and modulator of synaptic transmission. The role of the isoprenoid pathway in lung diseases and its relation to hemispheric dominance was assessed in this study. The following parameters were measured in patients with (i) bronchial asthma, (ii) chronic bronchitis emphysemia, (iii) idiopathic pulmonary fibrosis, (iv) sarcoidosis, and (v) in individuals with right hemispheric, left hemispheric and bihemispheric dominance: 1. plasma HMG CoA reductase, digoxin, dolichol, ubiquinone, and magnesium levels, 2. tryptophan, tyrosine catabolic patterns, 3. free radical metabolism, 4. glycoconjugate metabolism, and 5. membrane composition. In patients with lung disease there was elevated digoxin synthesis, increased dolichol and glycoconjugate levels, and low ubiquinone and elevated free radical levels. The RBC membrane Na+-K+ ATPase activity and serum magnesium were decreased. There was also an increase in tryptophan catabolites and reduction in tyrosine catabolites in the serum. There was an increase in cholesterol:phospholipid ratio and a reduction in glycoconjugate level of RBC membrane in these patients. The same biochemical patterns were obtained in individuals with right hemispheric chemical dominance. An upregulated isoprenoid pathway and hyperdigoxinemia are characteristic of lung disease and right hemispheric chemical dominance. Right hemispheric chemical dominance is important in deciding the predisposition to lung disease.

Reprints and Corporate Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

To request a reprint or corporate permissions for this article, please click on the relevant link below:

Academic Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

Obtain permissions instantly via Rightslink by clicking on the button below:

If you are unable to obtain permissions via Rightslink, please complete and submit this Permissions form. For more information, please visit our Permissions help page.