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Millimeter wave‐induced suppression of B16 F10 melanoma growth in mice: Involvement of endogenous opioids
Author(s) -
Radzievsky A.A.,
Gordiienko O.V.,
Szabo I.,
Alekseev S.I.,
Ziskin M.C.
Publication year - 2004
Publication title -
bioelectromagnetics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.435
H-Index - 81
eISSN - 1521-186X
pISSN - 0197-8462
DOI - 10.1002/bem.20018
Subject(s) - endogenous opioid , melanoma , endogeny , medicine , (+) naloxone , cell growth , subcutaneous injection , opioid , receptor , pharmacology , endocrinology , cancer research , chemistry , biochemistry
Abstract Millimeter wave treatment (MMWT) is widely used in Eastern European countries, but is virtually unknown in Western medicine. Among reported MMWT effects is suppression of tumor growth. The main aim of the present “blind” and dosimetrically controlled experiments was to evaluate quantitatively the ability of MMWT to influence tumor growth and to assess whether endogenous opioids are involved. The murine experimental model of B16 F10 melanoma subcutaneous growth was used. MMWT characteristics were: frequency, 61.22 GHz; average incident power density, 13.3 × 10 −3 W/cm 2 ; single exposure duration, 15 min; and exposure area, nose. Naloxone (1 mg/kg, intraperitoneally, 30 min prior to MMWT) was used as a nonspecific blocker of opioid receptors. Five daily MMW exposures, if applied starting at the fifth day following B16 melanoma cell injection, suppressed subcutaneous tumor growth. Pretreatment with naloxone completely abolished the MMWT‐induced suppression of melanoma growth. The same course of 5 MMW treatments, if started on day 1 or day 10 following tumor inoculations, was ineffective. We concluded that MMWT has an anticancer therapeutic potential and that endogenous opioids are involved in MMWT‐induced suppression of melanoma growth in mice. However, appropriate indications and contraindications have to be developed experimentally before recommending MMWT for clinical usage. Bioelectromagnetics 25:466–473, 2004. © 2004 Wiley‐Liss, Inc.