Effects of L-dopa and p-coumaric acid combination on oxidative stress, DNA damage, and mitochondrial apoptosis in neuroblastoma cells
DOI:
https://doi.org/10.3329/bjp.v18i2.65531Keywords:
Apoptosis, p-Coumaric acid, DNA damage, L-Dopa, MTT assay, Neuroblastoma cell, Oxidative stressAbstract
This study aimed to investigate the effects of levodopa (L-dopa), p-coumaric acid, and combinations in the neuroblastoma (N1E-115) cell. L-dopa and L-dopa plus p-coumaric acid group caused oxidative stress by increasing 12.5 and 3.7-fold in superoxide dismutase gene, 11.5 and 4.8-fold increase in catalase gene, respectively. In L-dopa and L-dopa plus p-coumaric acid application, p21 gene expression increased 1.3-fold and 3.2-fold, and the cell cycle stopped in the G1 phase in response to stress in the treatment groups. In the application of L-dopa plus p-coumaric acid to N1E-115 cells, the BCL-2 gene, which is an apoptosis inhibitor, was suppressed and the BAX gene increased 13-fold compared to the control. As a result, it was determined that the cytotoxic effect of L-dopa plus p-coumaric acid application was less than the individual application of the substances, and p-coumaric acid had an inhibitory effect on L-dopa-induced stress.
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Adamczyk B, Tharmalingam T, Rudd PM. Glycans as cancer biomarkers. Biochim Biophys Acta. 2012; 1820: 47-53.
Anden NE, Hfuxe K, Hamberger B, Hokfelt T. A quantitative study on the nigro-neostriatal dopamine neuron system in the rat. Acta Physiol Scand. 1966; 67: 106-12.
Annis MG, Soucie EL, Dlugosz PJ, Cruz‐Aguado JA, Penn LZ, Leber B, Andrews DW. Bax forms multispanning monomers that oligomerize to permeabilize membranes during apoptosis. EMBO J. 2005; 24: 2096-03.
Bahuguna A, Khan I, Bajpai VK, Kang SC. MTT assay to evaluate the cytotoxic potential of a drug. Bangladesh J Pharmacol. 2017; 12: 115-18.
Basma AN, Morris EJ, Nicklas WJ, Geller HM. L-dopa cytotoxicity to PC12 cells in culture is via its autoxidation. J Neurochem. 1995; 64: 825-32.
Blunt SB, Jenner P, Marsden CD. Suppressive effect of L-dopa on dopamine cells remaining in the ventral tegmental area of rats previously exposed to the neurotoxin 6-hydroxy-dopamine. Mov Disord. 1993; 8: 29-33.
Brenner C, Grimm S. The permeability transition pore complex in cancer cell death. Oncogene 2006; 25: 744-56.
Brenner C, Moulin M. Physiological roles of the permeability transition pore. Circ Res. 2012; 111:237-47.
Chien MM, Zahradka KE, Newell MK, Freed JH. Fas-induced B cell apoptosis requires an increase in free cytosolic magnesium as an early event. J Biol Chem. 1999; 274:059-66.
Cohen G. Monoamine oxidase and oxidative stress at dopami-nergic synapses. J Neural Transm Suppl. 1990; 32: 29-38.
Cohen G. Monoamine oxidase, hydrogen peroxide, and Parkinson's disease. Adv Neurol. 1987; 45: 19-25.
Cohen G. The pathobiology of Parkinson's disease: Biochemical aspects of dopamine neuron senescence. J Neural Transm Suppl. 1983; 19: 89-03.
Fernández-Salas E, Suh KS, Speransky VV, Bowers WL, Levy JM, Adams T, Pathak KR, Edwards LE, Hayes DD, Cheng C, Steven AC. mtCLIC/CLIC4, an organellular chloride channel protein, is increased by DNA damage and participates in the apoptotic response to p53. Mol Cell Biol. 2002; 22: 610-20.
German DC, Manaye K, Smith WK, Woodward DJ, Saper CB. Midbrain dopaminergic cell loss in Parkinson's disease: Computer visualization. Ann Neurol. 1989; 26: 107-14.
Hornykiewicz O. Dopamine (3-hydroxytyramine) and brain function. Pharmacol Rev. 1966; 18: 25-64.
Hornykiewicz O. Neurochemical pathology and the etiology of Parkinson's disease: Basic facts and hypothetical possibili-ties. Mt Sinai J Med. 1988; 55: 11-20.
Hornykiewicz O. Parkinson's disease: From brain homogenate to treatment. Fed Proc. 1973; 32: 83-90.
Javadov S, Hunter JC, Barreto-Torres G, Parodi-Rullan R. Targeting the mitochondrial permeability transition: Cardiac ischemia-reperfusion versus carcinogenesis. Cell Physiol Biochem. 2011; 27: 179-90.
Kianmehr Z, Khorsandi K, Mohammadi M, Hosseinzadeh R. Low-level laser irradiation potentiates anticancer activity of p-coumaric acid against human malignant melanoma cells. Melanoma Res. 2020; 30: 36-46.
Kushner BH. Neuroblastoma: A disease requiring a multitude of imaging studies. J Nucl Med. 2004; 45: 72-88.
Leanza L, Biasutto L, Manago A, Gulbins E, Zoratti M, Szabo I. Intracellular ion channels and cancer. Front Physiol. 2013; 4: 227.
Lonergan GJ, Schwab CM, Suarez ES, Carlson CL. Neuroblastoma, ganglioneuroblastoma, and ganglioneuroma: Radiologic-pathologic correlation. Radiographics 2002; 22: 11-34.
Naumowicz M, Kusaczuk M, Kruszewski MA, Gal M, Krętowski R, Cechowska-Pasko M, Kotyńska J. The modulating effect of lipid bilayer/p-coumaric acid interactions on electrical properties of model lipid membranes and human glioblastoma cells. Bioorg Chem. 2019; 92: 103-42.
Oberley LW, Buettner GR. Role of superoxide dismutase in cancer: A review. Cancer Res. 1979; 39: 41-49.
Ogawa N, Edamatsu R, Mizukawa K, Asanuma M, Kohno M, Mori A. Degeneration of dopaminergic neurons and free radicals. Possible participation of levodopa. Adv Neurol. 1993; 60: 42-50.
Ossio R, Roldan-Marin R, Martinez-Said H, Adams DJ, Robles-Espinoza CD. Melanoma: A global perspective. Nat Rev Cancer. 2017; 17: 93-04.
Park JG, Frucht H, LaRocca RV, Bliss Jr DP, Kurita Y, Chen TR, Henslee JG, Trepel JB, Jensen RT, Johnson BE, Bang YJ. Characteristics of cell lines established from human gastric carcinoma. Cancer Res. 1990; 50: 73-80.
Pawelek JM, Lerner AB. 5,6-Dihydroxyindole is a melanin precursor showing potent cytotoxicity. Nature 1978; 276: 26-28.
Pedrosa R, Soares-da-Silva P. Oxidative and non-oxidative mechanisms of neuronal cell death and apoptosis by L-3,4-dihydroxyphenylalanine (L-DOPA) and dopamine. Br J Pharmacol. 2002; 137: 305-13.
Rha SE, Byun JY, Jung SE, Chun HJ, Lee HG, Lee JM. Neurogenic tumors in the abdomen: Tumor types and imaging characteristics. Radiographics 2003; 23: 29-43.
Szabó I, Bock J, Grassmé H, Soddemann M, Wilker B, Lang F, Zoratti M, Gulbins E. Mitochondrial potassium channel Kv1.3 mediates Bax-induced apoptosis in lymphocytes. Proc Natl Acad Sci USA. 2008; 105: 861-66.
Szabo I, Soddemann M, Leanza L, Zoratti M, Gulbins E. Single-point mutations of a lysine residue change function of Bax and Bcl-xL expressed in Bax- and Bak-less mouse embryonic fibroblasts: novel insights into the molecular mechanisms of Bax-induced apoptosis. Cell Death Differ. 2011; 18: 427-38.
Vauzour D, Corona G, Spencer JP. Caffeic acid, tyrosol and p-coumaric acid are potent inhibitors of 5-S-cysteinyl-dopamine induced neurotoxicity. Arch Biochem Biophys. 2010; 501: 106-11.
Yan X, Chen X, Xu X, Liu J, Fu C, Zhao D, Zhao W, Ma R, Sun L. Mechanism underlying p-coumaric acid alleviation of lipid accumulation in palmitic acid-treated human hepatoma cells. J Agric Food Chem. 2020; 68: 742-49.
Zoratti M, De Marchi U, Gulbins E, Szabo I. Novel channels of the inner mitochondrial membrane. Biochim Biophys Acta. 2009; 1787: 351-63.
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