Plasma Prolidase Activity and Oxidative Stress in Patients with Parkinson's Disease

Akhilesh Kumar Verma, Janak Raj, Vivek Sharma, Tej Bali Singh, Shalabh Srivastava, Ragini Srivastava, Akhilesh Kumar Verma, Janak Raj, Vivek Sharma, Tej Bali Singh, Shalabh Srivastava, Ragini Srivastava

Abstract

Prolidase deficiency has been related to mental retardation and oxidative stress. The study aimed to observe plasma prolidase activity (PPA), total oxidant status (TOS), total antioxidant status (TAS), and oxidative stress index (OSI) in patients with Parkinson's disease (PD). 240 subjects with PD and 150 healthy volunteers were considered as cases and controls, respectively. PPA, TOS, TAS, and OSI were measured spectrophotometrically. PPA and TAS in cases were more significantly decreased than controls (P < 0.01), while TOS and OSI were significantly increased (P < 0.001). In cases, nonsignificant, positive correlation was observed between PPA and TOS and OSI while significant, negative correlation was observed between PPA and TAS (P = 0.047). PPA in cases was nonsignificantly decreased with increased duration of PD (P = 0.747) while TAS was significantly decreased (P < 0.001) and TOS and OSI were significantly increased (P < 0.001). It was observed that higher age groups had decreased PPA, and TAS and increased TOS and OSI compared to lower age groups in cases. In summary, patients with PD have decreased PPA and increased oxidative stress compared to healthy volunteers. PPA was associated with oxidative stress markers in patients with PD. Decreased PPA and TAS and increased TOS and OSI were associated with progression of disease and higher age.

References

    1. Savitt J. M., Dawson V. L., Dawson T. M. Diagnosis and treatment of Parkinson disease: molecules to medicine. Journal of Clinical Investigation. 2006;116(7):1744–1754. doi: 10.1172/jci29178.
    1. Moore D. J., West A. B., Dawson V. L., Dawson T. M. Molecular pathophysiology of Parkinson's disease. Annual Review of Neuroscience. 2005;28:57–87. doi: 10.1146/annurev.neuro.28.061604.135718.
    1. Beal M. F. Mitochondria, oxidative damage, and inflammation in Parkinson's disease. Annals of the New York Academy of Sciences. 2003;991:120–131.
    1. Hirsch E. C., Vyas S., Hunot S. Neuroinflammation in Parkinson's disease. Parkinsonism and Related Disorders. 2012;18(supplement 1):S210–S212. doi: 10.1016/S1353-8020(11)70065-7.
    1. Surażynski A., Miltyk W., Palka J., Phang J. M. Prolidase-dependent regulation of collagen biosynthesis. Amino Acids. 2008;35(4):731–738. doi: 10.1007/s00726-008-0051-8.
    1. Türkbeyler I., Demir T., Pehlivan Y., et al. Prolidase could Act as a diagnosis and treatment mediator in lung fibrosis. Inflammation. 2012;35(5):1747–1752. doi: 10.1007/s10753-012-9493-y.
    1. Arikanoglu A., Akil E., Varol S., et al. Relationship of cognitive performance with prolidase and oxidative stress in Alzheimer disease. Neurological Sciences. 2013;34(12):2117–2121. doi: 10.1007/s10072-013-1346-4.
    1. Uzar E., Tamam Y., Evliyaoglu O., et al. Serum prolidase activity and oxidative status in patients with diabetic neuropathy. Neurological Sciences. 2012;33(4):875–880. doi: 10.1007/s10072-011-0857-0.
    1. Selek S., Altindag A., Saracoglu G., Celik H., Aksoy N. Prolidase activity and its diagnostic performance in bipolar disorder. Journal of Affective Disorders. 2011;129(1-3):84–86. doi: 10.1016/j.jad.2010.09.003.
    1. Erbağci A. B., Araz M., Tarakçioğlu M., Namiduru E. S. Serum prolidase activity as a marker of osteoporosis in type 2 diabetes mellitus. Clinical Biochemistry. 2002;35(4):263–268. doi: 10.1016/s0009-9120(02)00305-3.
    1. Kumari S., Verma A. K., Rungta S., Mitra R., Srivastava R., Kumar N. Serum prolidase activity, oxidant and antioxidant status in nonulcer dyspepsia and healthy volunteers. ISRN Biochemistry. 2013;2013:6. doi: 10.1155/2013/182601.182601
    1. Mantle D., Falkous G., Ishiura S., Blanchard P. J., Perry E. K. Comparison of proline endopeptidase activity in brain tissue from normal cases and cases with Alzheimer's disease, Lewy body dementia, Parkinson's disease and Huntington's disease. Clinica Chimica Acta. 1996;249(1-2):129–139. doi: 10.1016/0009-8981(96)06282-1.
    1. Kirbas A., Kirbas S., Cure M. C., Tufekci A. Paraoxonase and arylesterase activity and total oxidative/anti-oxidative status in patients with idiopathic Parkinson's disease. Journal of Clinical Neuroscience. 2014;21(3):451–455. doi: 10.1016/j.jocn.2013.04.025.
    1. Verma A. K., Chandra S., Singh R. G., Singh T. B., Srivastava S., Srivastava R. Serum prolidase activity and oxidative stress in diabetic nephropathy and end stage renal disease: a correlative study with glucose and creatinine. Biochemistry Research International. 2014;2014:7. doi: 10.1155/2014/291458.291458
    1. Erel O. A novel automated method to measure total antioxidant response against potent free radical reactions. Clinical Biochemistry. 2004;37(2):112–119. doi: 10.1016/j.clinbiochem.2003.10.014.
    1. Erel O. A new automated colorimetric method for measuring total oxidant status. Clinical Biochemistry. 2005;38(12):1103–1111. doi: 10.1016/j.clinbiochem.2005.08.008.
    1. Mitsubuchi H., Nakamura K., Matsumoto S., Endo F. Inborn errors of proline metabolism. Journal of Nutrition. 2008;138(10):2016S–2020S.
    1. Gomes I., Xiong W., Miki T., Rosner M. R. A proline- and glutamine-rich protein promotes apoptosis in neuronal cells. Journal of Neurochemistry. 1999;73(2):612–622. doi: 10.1046/j.1471-4159.1999.0730612.x.
    1. Pettmann B., Henderson C. E. Neuronal cell death. Neuron. 1998;20(4):633–647. doi: 10.1016/S0896-6273(00)81004-1.
    1. Wang Y., Meriin A. B., Zaarur N., et al. Abnormal proteins can form aggresome in yeast: aggresome-targeting signals and components of the machinery. The FASEB Journal. 2009;23(2):451–463. doi: 10.1096/fj.08-117614.
    1. Sherman M. Y., Goldberg A. L. Cellular defenses against unfolded proteins: a cell biologist thinks about neurodegenerative diseases. Neuron. 2001;29(1):15–32. doi: 10.1016/s0896-6273(01)00177-5.
    1. McNaught K. S. P., Shashidharan P., Perl D. P., Jenner P., Olanow C. W. Aggresome-related biogenesis of Lewy bodies. European Journal of Neuroscience. 2002;16(11):2136–2148. doi: 10.1046/j.1460-9568.2002.02301.x.
    1. Shea T. B., Zheng Y.-L., Ortiz D., Pant H. C. Cyclin-dependent kinase 5 increases perikaryal neurofilament phosphorylation and inhibits neurofilament axonal transport in response to oxidative stress. Journal of Neuroscience Research. 2004;76(6):795–800. doi: 10.1002/jnr.20099.
    1. Sobue G., Hashizume Y., Yasuda T., et al. Phosphorylated high molecular weight neurofilament protein in lower motor neurons in amyotrophic lateral sclerosis and other neurodegenerative diseases involving ventral horn cells. Acta Neuropathologica. 1990;79(4):402–408. doi: 10.1007/bf00308716.
    1. Ikeda K., Nakamura Y., Kiyozuka T., et al. Serological profiles of urate, paraoxonase-1, ferritin and lipid in Parkinson's disease: changes linked to disease progression. Neurodegenerative Diseases. 2011;8(4):252–258. doi: 10.1159/000323265.
    1. Miller R. L., James-Kracke M., Sun G. Y., Sun A. Y. Oxidative and inflammatory pathways in Parkinson's disease. Neurochemical Research. 2009;34(1):55–65. doi: 10.1007/s11064-008-9656-2.
    1. Betarbet R., Sherer T. B., Greenamyre J. T. Ubiquitin-proteasome system and Parkinson's diseases. Experimental Neurology. 2005;191(supplement 1):S17–S27. doi: 10.1016/j.expneurol.2004.08.021.
    1. Kok P. L., Shan H. H., de Silva R., Tan B. K. H., Yi Z. Z. Oxidative stress: apoptosis in neuronal injury. Current Alzheimer Research. 2006;3(4):327–337. doi: 10.2174/156720506778249515.
    1. Serafini M., del Rio D. Understanding the association between dietary antioxidants, redox status and disease: is the total antioxidant capacity the right tool? Redox Report. 2004;9(3):145–152. doi: 10.1179/135100004225004814.
    1. Sharma A., Kaur P., Kumar B., Prabhakar S., Gill K. D. Plasma lipid peroxidation and antioxidant status of Parkinson's disease patients in the Indian population. Parkinsonism and Related Disorders. 2008;14(1):52–57. doi: 10.1016/j.parkreldis.2007.06.009.
    1. Hattiangady B., Kuruba R., Shetty A. K. Acute seizures in old age leads to a greater loss of CA1 pyramidal neurons, an increased propensity for developing chronic TLE and a severe cognitive dysfunction. Aging and Disease. 2011;2(1):1–17.
    1. Cheng H.-C., Ulane C. M., Burke R. E. Clinical progression in Parkinson disease and the neurobiology of axons. Annals of Neurology. 2010;67(6):715–725. doi: 10.1002/ana.21995.
    1. van den Eeden S. K., Tanner C. M., Bernstein A. L., et al. Incidence of Parkinson's disease: variation by age, gender, and race/ethnicity. The American Journal of Epidemiology. 2003;157(11):1015–1022. doi: 10.1093/aje/kwg068.

Source: PubMed

Sponsorer och medarbetare

Medicinska tillstånd

Läkemedelsinterventioner

3
Prenumerera