Significantly Reduced Salivary Nitric Oxide Synthesis in Patients with Parkinson’s Disease

Huskić, Jasminko; Paperniku, Alma; Husić, Azra; Alendar, Faruk; Mulabegović, Nedžad

doi:10.17305/bjbms.2005.3277

Cited by 8 publications

(16 citation statements)

References 10 publications

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“…Further experimentation will determine whether high‐throughput ELISA for salivary HO‐1 in PD and other conditions will necessitate concomitant measurement of AMY1A protein. Hyper‐ or hyposialorrhea may arise in PD individuals as autonomic nervous system manifestations of the disease attributed to uncoordinated deglutition and pooling of saliva within the oropharynx and following treatment with pro‐DA or anticholinergic medications . Though no correlations have been reported between hyper‐ or hyposialorrhea and salivary biomarker levels, future studies of HO‐1 as a potential biomarker for idiopathic PD should assess whether these levels are affected by salivary secretion rates.…”

Section: Discussionmentioning

confidence: 99%

Evaluation of salivary heme oxygenase‐1 as a potential biomarker of early Parkinson's disease

et al. 2018

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Section: Discussionmentioning

confidence: 99%

Evaluation of salivary heme oxygenase‐1 as a potential biomarker of early Parkinson's disease

et al. 2018

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“…Notably, NO levels in PD are ambiguous and studies on nitrite and nitrate measurements in the cerebrospinal fluid (CSF) of PD patients have been contradictory, as there was no change [ 37 ], increase [ 38 ] or decrease [ 39 , 40 ]. On the other hand, some studies have shown that CSF and plasma nitrate levels did not correlate with age at onset, duration, scores of the unified Parkinson’s disease rating scales, and Hoehn and Yahr staging in the patients group [ 37 , 41 ].…”

Section: Discussionmentioning

confidence: 99%

Iron and Oxidative Stress in Parkinson’s Disease: An Observational Study of Injury Biomarkers

et al. 2016

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Parkinson's disease (PD) is characterized by progressive motor impairment attributed to progressive loss of dopaminergic neurons in the substantia nigra (SN) pars compacta. In addition to an accumulation of iron, there is also an increased production of reactive oxygen/nitrogen species (ROS/RNS) and inflammatory markers. These observations suggest that iron dyshomeostasis may be playing a key role in neurodegeneration. However, the mechanisms underlying this metal-associated oxidative stress and neuronal damage have not been fully elucidated. To determine peripheral levels of iron, ferritin, and transferrin in PD patients and its possible relation with oxidative/nitrosative parameters, whilst attempting to identify a profile of peripheral biomarkers in this neurological condition. Forty PD patients and 46 controls were recruited to compare serum levels of iron, ferritin, transferrin, oxidative stress markers (superoxide dismutase (SOD), catalase (CAT), nitrosative stress marker (NOx), thiobarbituric acid reactive substances (TBARS), non-protein thiols (NPSH), advanced oxidation protein products (AOPP), ferric reducing ability of plasma (FRAP) and vitamin C) as well as inflammatory markers (NTPDases, ecto-5’-nucleotidase, adenosine deaminase (ADA), ischemic-modified albumin (IMA) and myeloperoxidase). Iron levels were lower in PD patients, whereas there was no difference in ferritin and transferrin. Oxidative stress (TBARS and AOPP) and inflammatory markers (NTPDases, IMA, and myeloperoxidase) were significantly higher in PD, while antioxidants FRAP, vitamin C, and non-protein thiols were significantly lower in PD. The enzymes SOD, CAT, and ecto-5’-nucleotidase were not different among the groups, although NOx and ADA levels were significantly higher in the controls. Our data corroborate the idea that ROS/RNS production and neuroinflammation may dysregulate iron homeostasis and collaborate to reduce the periphery levels of this ion, contributing to alterations observed in the pathophysiology of PD.

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“…However, Huerta et al found no association among PD and three polymorphisms in the eNOS, nNOS and iNOS genes ( 38 ). Furthermore, significantly low circulating levels of NO and reduced salivary NOS were demonstrated in patients with PD ( 39 , 40 ). Chronic administration of rotenone was found to increase the NO levels in the cortex and striatum of rats, leading to significant injury in the nigrostriatal pathway ( 18 , 19 ).…”

Section: Discussionmentioning

confidence: 99%

Excessive levels of nitric oxide in rat model of Parkinson’s disease induced by rotenone

Xiong

Lang

et al. 2014

Experimental and Therapeutic Medicine

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Systemic rotenone models of Parkinson’s disease (PD) are highly reproducible and may provide evidence on the pathogenesis of PD. In the present study, male Sprague-Dawley rats (1-year-old) were subcutaneously administered with rotenone (1.5 mg/kg/day) for six days and observed for the following three weeks. Compared with the control rats, a significant decrease was observed in the body weight and a marked increase was observed in the areas under the behavioral scoring curves in the rotenone-treated rats. Immunohistochemical staining revealed that the abundance of nigral tyrosine hydroxylase (TH)-positive neurons was markedly reduced following rotenone treatment. ELISA and neurochemical assays demonstrated a significant increase in the levels of nitric oxide (NO) and NO synthase, whereas a marked decrease was observed in the thiol levels in the brains of the rotenone-treated rats. Thus, subacute rotenone treatment was found to induce behavioral deficits and the loss of nigral TH-positive neurons which may be associated with the excessive levels of NO in the rat brains.

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Significantly Reduced Salivary Nitric Oxide Synthesis in Patients with Parkinson’s Disease

Cited by 8 publications

References 10 publications

Evaluation of salivary heme oxygenase‐1 as a potential biomarker of early Parkinson's disease

Evaluation of salivary heme oxygenase‐1 as a potential biomarker of early Parkinson's disease

Iron and Oxidative Stress in Parkinson’s Disease: An Observational Study of Injury Biomarkers

Excessive levels of nitric oxide in rat model of Parkinson’s disease induced by rotenone

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