It is well known that oxidative stress damages bimolecules such as DNA and lipids. No study is available on the morphine-induced oxidative damage and fatty acids changes in brain and spinal tissues. The aim of this work was to determine the effects of morphine on the concentrations and compositions of fatty acid in spinal cord segments and brain tissues in rabbits as well as lipid peroxidation (LP) and glutathione (GSH) levels in cortex brain.
Twelve New Zealand albino rabbits were used and they were randomly assigned to two groups of 6 rabbits each. First group used as control although morphine administrated to rats in second group. Cortex brain and (cervical, thoracic, lumbar) samples were taken.
The fatty acids between n:18.0 and 21.0 were present in spinal cord sections and n:10 fatty acids in control animals were present in the brain tissues. Compared to n:20.0–24.0 fatty acids in spinal cord sections and 8.0 fatty acids in the brain tissues of drug administered animals. The concentration and composition of the fatty acid methyl esters in spinal cord and brain tissues was decreased by morphine treatments. LP levels in the cortex brain were increased although GSH levels were decreased by the morphine administration.
In conclusion, unsaturated fatty acids contents in brain and spinal cord sections and GSH were reduced by administrating spinal morphine although oxidative stress as LP increased. The inhibition oxidative damage may be a useful strategy for the development of a new protection for morphine administration as well as opiate abuse.
Halliwell B, Gutteridge JMC (1999) Free radicals, other reactive species and disease. In Free Radicals in Biology and Medicine, 3rd ed. Halliwell B, Gutteridge JMC, eds, Oxford University Press, New York, pp 639–645Google Scholar
Nazıroğlu M (2006) Effects of physical exercise with a dietary vitamins C and E combination on oxidative stress in muscle, liver and brain of streptozotocin- induced diabetic pregnant rat. Vitamin E: New Research. Ed. MH Braunstain, Nova Science Publishers Inc., NY, USA. pp 69–83Google Scholar
Guzman DC, Vazquez IE, Brizuela NO, Alvarez RG, Mejia GB, Garcia EH, Santamaria D, de Apreza MR, Olguin HJ (2006) Assessment of oxidative damage induced by acute doses of morphine sulfate in postnatal and adult rat brain. Neurochem Res 31:549–554PubMedCrossRefGoogle Scholar
Xu B, Wang Z, Li G, Li B, Lin H, Zheng R, Zheng Q. (2006) Heroin-administered mice involved in oxidative stress and exogenous antioxidant-alleviated withdrawal syndrome. Basic Clin Pharmacol Toxicol. 99:153–161PubMedCrossRefGoogle Scholar
Zhang YT, Zheng QS, Pan J, Zheng RL. (2004) Oxidative damage of biomolecules in mouse liver induced by morphine and protected by antioxidants. Basic Clin Pharmacol Toxicol. 95:53–58PubMedGoogle Scholar
Nazıroğlu M, Brandsch C. (2006) Dietary hydrogenated soybean oil affects lipid and vitamin E metabolism in rats. J Nutr Sci Vitaminol (Tokyo). 52:83–88, 2006Google Scholar
Yilmaz O, Celik S, Cay M, Naziroglu M. (1997) Protective role of intraperitoneally administrated vitamin E and selenium on the levels of total lipid, total cholesterol, and fatty acid composition of muscle and liver tissues in rats. Cell Biochem 64:233–241CrossRefGoogle Scholar
Celik S, Yilmaz O, Asan T, Naziroglu M, Cay M, Aksakal M. (1999) Influence of dietary selenium and vitamin E on the levels of fatty acids in brain and liver tissues of lambs. Cell Biochem Funct 17:115–121PubMedCrossRefGoogle Scholar
Sherlock Microbial Identification System (version 4.0), MIS Operating manual, 145 pp, MIDI, Inc, Newark, DE, USAGoogle Scholar
Mercandate S. (1999) Problems of long-term spinal opioid treatment in advanced cancer patients. Pain 79:1–13CrossRefGoogle Scholar
Wagemans MF, van der Valk P, Spoelder EM, Zuurmond WW, de Lange JJ (1997) Neurohistopathological findings after continuous intrathecal administration of morphine or a morphine/bupivacaine mixture in cancer pain patients. Acta Anaesthesiol Scand 41:1033–1038PubMedCrossRefGoogle Scholar
Hodgson PS, Neal JM, Pollock JE, Liu SS (1999) The neurotoxicity of drugs given intrathecally (spinal). Anesth Analg 88:797–809PubMedCrossRefGoogle Scholar
Yaksh TL, Noueihed RY, Durant PA (1986) Studies of the pharmacology and pathology of intrathecally administered 4-anilinopiperidine analogues and morphine in the rat and cat. Anesthesiology 64:54–66, 1986PubMedCrossRefGoogle Scholar
Alici HA, Ozmen I, Cesur M, Sahin F (2003) Effect of the spinal drug tramadol on the fatty acid compositions of rabbit spinal cord and brain. Biol Pharm Bull 26:1403–1406PubMedCrossRefGoogle Scholar
Placer ZA, Cushman L, Johnson BC (1966) Estimation of products of lipid peroxidation (malonyl dialdehyde) in biological fluids. Anal Biochem 16:359–364PubMedCrossRefGoogle Scholar
Sedlak J, Lindsay RHC (1968) Estimation of total, protein bound and non-protein sulfhydryl groups in tissue with Ellmann’ s reagent. Anal Biochem 25:192–205PubMedCrossRefGoogle Scholar
Lowry OH, Rosebrough NJ, Farr AL, Randall RJ (1951) Protein measurement with the Folin- Phenol reagent. J Biol Chem 193:265–275PubMedGoogle Scholar
Di Chiara G, Imperato A. (1988) Drugs abused by humans preferentially increase synaptic dopamine concentrations in the mesolimbic system of freely moving rats. Proc Natl Acad Sci USA. 85:5274–5278PubMedCrossRefGoogle Scholar
Singhal PC, Pamarthi M, Shah R, Chandra D, Gibbons N (1994) Morphine stimulates superoxide formation by glomerular mesangial cells. Inflammation. 18:293–299PubMedCrossRefGoogle Scholar
Di Bello MG, Masini E, Ioannides C, Fomusi Ndisang J, Raspanti S, Bani Sacchi T, Mannaioni PF (1998) Histamine release from rat mast cells induced by the metabolic activation of drugs of abuse into free radicals. Inflamm Res. 47:122–130PubMedCrossRefGoogle Scholar
Goudas LC, Langlade A, Serrie A, Matson W, Milbury P, Thurel C, Sandouk P, Carr DB. (1999). Acute decreases in cerebrospinal fluid glutathione levels after intracerebroventricular morphine for cancer pain. Anesth Analg. 89:1209–1215PubMedCrossRefGoogle Scholar
Farooqui AA, Yi Ong W, Lu XR, Halliwell B, Horrocks LA. (2001) Neurochemical consequences of kainate-induced toxicity in brain: involvement of arachidonic acid release and prevention of toxicity by phospholipase A(2) inhibitors. Brain Res Brain Res Rev 38:61–78PubMedCrossRefGoogle Scholar