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Diethyldithiocarbamate and brain copper

P Allain¹, N Krari

¹Laboratoire de Pharmacologie et Toxicologie, Centre Hospitalier Universitaire, Angers, France.

Research Communications in Chemical Pathology and Pharmacology

|April 1, 1993

Summary

Diethyldithiocarbamate (DEDTC) increases brain copper levels, but not through a copper-DEDTC complex crossing the blood-brain barrier. This finding suggests alternative mechanisms are responsible for copper accumulation in the brain.

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Area of Science:

Neuroscience
Toxicology
Biochemistry

Background:

Diethyldithiocarbamate (DEDTC) is known to affect copper levels in the brain.
The mechanism by which DEDTC influences brain copper remains unclear.
A proposed mechanism involves the formation of a DEDTC-copper complex that can cross the blood-brain barrier.

Purpose of the Study:

To investigate the hypothesis that DEDTC-induced increases in brain copper are mediated by a lipophilic DEDTC-copper complex.
To compare the effects of DEDTC alone, DEDTC with copper, and a pre-formed DEDTC-copper complex on rat brain copper concentrations.

Main Methods:

Rats were administered DEDTC alone, DEDTC with copper, or a DEDTC-copper complex daily for three weeks.
Time-course effects of single administrations of DEDTC and the DEDTC-copper complex were analyzed.
Brain copper concentrations were measured at various time points post-administration.

Main Results:

Daily administration of DEDTC, DEDTC with copper, or the DEDTC-copper complex resulted in similar increases in brain copper levels.
Single administration of DEDTC or the DEDTC-copper complex induced a delayed increase in brain copper, persisting for at least three days.
Supplementation with additional copper did not enhance the effect of DEDTC on brain copper levels.

Conclusions:

The formation of a DEDTC-copper complex that readily crosses the blood-brain barrier is unlikely to be the primary mechanism for DEDTC-induced brain copper increase.
The observed delayed increase in brain copper suggests complex pharmacokinetic or pharmacodynamic processes are involved.
Alternative mechanisms, beyond direct copper chelation and transport, may explain DEDTC's impact on brain copper homeostasis.

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