Stanley Jacob

Pharmacology of DMSO

A wide range of primary pharmacological actions of dimethyl sulfoxide (DMSO) has been documented in laboratory studies: membrane penetration, membrane transport, effects on connective tissue, anti-inflammation, nerve blockade (analgesia), bacteriostasis, diuresis, enhancement or reduction of the effectiveness of other drugs, cholinesterase inhibition, nonspecific enhancement of resistance to infection, vasodilation, muscle relaxation, antagonism to platelet aggregation, and influence on serum cholesterol in experimental hypercholesterolemia. This substance induces differentiation and function of leukemic and other malignant cells. DMSO also has prophylactic radioprotective properties and cryoprotective actions. It protects against ischemic injury.

Pharmacology of dimethyl sulfoxide in cardiac and CNS damage

The pharmacological effects of dimethyl sulfoxide (DMSO) administration include some desirable properties that may be useful in the treatment of medical disorders resulting in tissue injury and compromised organ systems. These properties include the reported effects of DMSO on impaired blood flow, suppression of cytotoxicity from excess glutamate release that may result in lethal NMDA-AMPA activation, restriction of cytotoxic Na(+) and Ca(2+) entry into damaged cells, blocking tissue factor (TF) from contributing to thrombosis, reduction of intracranial pressure, tissue edema, and inflammatory reactions, and inhibition of vascular smooth muscle cell migration and proliferation that can lead to atherosclerosis of the coronary, peripheral, and cerebral circulation. A review of the basic and clinical literature on the biological actions of DMSO in cardiac and central nervous system (CNS) damage or dysfunction indicates that this agent, alone or in combination with other synergistic molecules, has been reported to neutralize or attenuate pathological complications that harmed or can further harm these two organ systems. The effects of DMSO make it potentially useful in the treatment of medical disorders involving head and spinal cord injury, stroke, memory dysfunction, and ischemic heart disease.

The absorption, metabolism and excretion of dimethyl sulfoxide by Rhesus monkeys

The absorption and excretion of dimethyl sulfoxide (DMSO) were studied in Rhesus monkeys (Macaca mulatta) given daily oral doses of 3 gms DMSO/kg B.W. for 14 days. DMSO and its major metabolite, dimethyl sulfone (DMSO2), were measured in serum, urine and feces by gas-liquid chromatography. DMSO was absorbed rapidly, reached a steady state blood level after 1 day and then was cleared from blood within 72 hrs after ending treatment. Serum DMSO declined in a linear fashion on semilogarithmic coordinates as described by second order kinetics. It had a half-life of 16 hrs. DMSO2 appeared in blood within 2 hrs and reached a steady state concentration after 4 days of treatment. DMSO2 was cleared from blood about 120 hrs after DMSO administration was stopped. Its half-life in blood was calculated to be 38 hrs. Urinary excretion of unmetabolized DMSO and DMSO2 accounted for about 60% and 16%, respectively, of the total ingested dose. Neither DMSO nor DMSO2 was detected in fecal samples. However, when added to fecal samples, DMSO was degraded rapidly. Although dimethyl sulfide (DMS) was not measured, some DMSO was metabolized to this compound because of the particular sweetness of breath of the monkeys. We conclude that the absorption of DMSO by monkeys is similar to that for humans, but that its conversion to DMSO2 and urinary elimination are more rapid in monkeys.

Dimethyl Sulfoxide (DMSO) in Trauma and Disease

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