Remarkable interest has risen in the idea that oxidative/nitrosative stress is mediated in the etiology of numerous human diseases. Oxidative/Nitrosative stress is the result of an disequilibrium in oxidant/antioxidant which reveals from continuous increase of Reactive Oxygen and Reactive Nitrogen Species production. The aim of this review is to emphasize with current information the importance of antioxidants which play the role in cellular responce against oxidative/nitrosative stress, which would be helpful in enhancing the knowledge of any biochemist, pathophysiologist, or medical personnel regarding this important issue. Products of lipid peroxidation have commonly been used as biomarkers of oxidative/nitrosative stress damage. Lipid peroxidation generates a variety of relatively stable decomposition end products, mainly α, β-unsaturated reactive aldehydes, such as malondialdehyde, 4-hydroxy-2-nonenal, 2-propenal (acrolein) and isoprostanes, which can be measured in plasma and urine as an indirect index of oxidative/nitrosative stress. Antioxidants are exogenous or endogenous molecules that mitigate any form of oxidative/nitrosative stress or its consequences. They may act from directly scavenging free radicals to increasing antioxidative defences. Antioxidant deficiencies can develop as a result of decreased antioxidant intake, synthesis of endogenous enzymes or increased antioxidant utilization. Antioxidant supplementation has become an increasingly popular practice to maintain optimal body function. However, antoxidants exhibit pro-oxidant activity depending on the specific set of conditions. Of particular importance are their dosage and redox conditions in the cell.

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The importance of antioxidants which play the role in cellular response against oxidative/nitrosative stress: current state

Despite intense investigation, the mechanisms of the different forms of trigeminal neuropathic pain remain substantially unidentified. The transient receptor potential ankyrin 1 channel (encoded by TRPA1 ) has been reported to contribute to allodynia or hyperalgesia in some neuropathic pain models, including those produced by sciatic nerve constriction. However, the role of TRPA1 and the processes that cause trigeminal pain-like behaviours from nerve insult are poorly understood. The role of TRPA1, monocytes and macrophages, and oxidative stress in pain-like behaviour evoked by the constriction of the infraorbital nerve in mice were explored. C57BL/6 and wild-type ( Trpa1+/+ ) mice that underwent constriction of the infraorbital nerve exhibited prolonged (20 days) non-evoked nociceptive behaviour and mechanical, cold and chemical hypersensitivity in comparison to sham-operated mice ( P < 0.05– P < 0.001). Both genetic deletion of Trpa1 ( Trpa1−/− ) and pharmacological blockade (HC-030031 and A-967079) abrogated pain-like behaviours (both P < 0.001), which were abated by the antioxidant, α-lipoic acid, and the nicotinamide adenine dinucleotide phosphate oxidase inhibitor, apocynin (both P < 0.001). Nociception and hypersensitivity evoked by constriction of the infraorbital nerve was associated with intra- and perineural monocytic and macrophagic invasion and increased levels of oxidative stress by-products (hydrogen peroxide and 4-hydroxynonenal). Attenuation of monocyte/macrophage increase by systemic treatment with an antibody against the monocyte chemoattractant chemokine (C-C motif) ligand 2 (CCL2) or the macrophage-depleting agent, clodronate (both P < 0.05), was associated with reduced hydrogen peroxide and 4-hydroxynonenal perineural levels and pain-like behaviours (all P < 0.01), which were abated by perineural administration of HC-030031, α-lipoic acid or the anti-CCL2 antibody (all P < 0.001). The present findings propose that, in the constriction of the infraorbital nerve model of trigeminal neuropathic pain, pain-like behaviours are entirely mediated by the TRPA1 channel, targeted by increased oxidative stress by-products released from monocytes and macrophages clumping at the site of nerve injury.

* Abbreviations
 : 4-HNE = : 4-hydroxynonenal
 AITC = : allyl isothiocyanate
 A-967079 = : (1 E ,3 E )-1-(4-Fluorophenyl)-2-methyl-1-penten-3-one oxime
 CION = : constriction of the infraorbital nerve
 HC-030031 = : (2-(1,3-Dimethyl-2,6-dioxo-1,2,3,6-tetrahydro-7H-purin-7-yl)- N -(4-isopropylphenyl) acetamide)
 LCL = : liposome-encapsulated clodronate

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TRPA1 mediates trigeminal neuropathic pain in mice downstream of monocytes/macrophages and oxidative stress.

Tinea pedis (TP) is an infection of the feet caused by fungi. The infectious diseases caused by dermatophytes are mainly related to the enzymes produced by these fungi. Up to the now, the local 8-iso-prostaglandin F2α (8-iso-PGF2α), concentration as oxidative stress biomarker and trace elements status have not been published in patients with TP. The aim of this study is to evaluate the relationship between oxidative stress and trace elements (Cu, Zn, Se), and to evaluate the ratios of Cu/Zn and Cu/Se in this disorder. Forty-three consecutive patients with a diagnosis of unilateral interdigital TP were enrolled in this study. The samples were obtained by scraping the skin surface. 8-iso-PGF2α concentrations in scraping samples were determined by ELISA. In addition, the levels of Se, Zn and Cu in scraping samples were determined on flame and furnace atomic absorption spectrophotometer using Zeeman background correction. Oxidative stress was confirmed by the significant elevation in 8-iso-PGF2α concentrations (p   0.05). Our results showed that there is a possible link between oxidative stress (increased 8-iso-PGF2α concentrations) and imbalanced of trace elements status in lesional area of TP patients. The use of antifungal agents together with both Zn and Se drugs could be helpful in the both regression of disease and in shortening the duration of disease.

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Evaluation of local trace element status and 8-Iso-prostaglandin F2α concentrations in patients with Tinea pedis

Acute, graded, nerve compression was applied to the sciatic nerves of 91 rats in whom an inflatable miniature Plexiglass compression device had been implanted in the thigh. The experiment was designed to study the pathogenesis of lesions in the nerve entrapment syndrome. Under general anesthesia, external pressures of 80 mm of Hg, 30 mm of Hg and 10 mm of Hg were used to compress nerves for 2 hours. Identical compression devices were placed around the contralateral sciatic nerves but remained uninflated so that these nerves could be used as controls. Nerves were excised at intervals of 4 and 24 hours, and at 1, 2, 5, 6, 7, 10, 14, and 28 days, and full thickness transverse sections were made from Araldite blocks. The first pathologic change was nerve edema which was observed at all time points and correlated with the severity of axonal injury. Axonal lesions were predominant in nerves exposed to 80 mm of Hg (7.5 +/- 1.9 nerve fibers per high power microscopic field (HPF)) while nerves compressed at 30 mm of Hg showed fewer damaged axons (2.6 +/- 1.4 per HPF). Demyelination was the predominant lesion in nerves subjected to 30 mm of Hg and was commonly present in nerves around which the compression chamber remained uninflated. Electron microscopy revealed demyelination to be associated with Schwann cell necrosis. The topography of nerve fiber injury was remarkable; subperineurial fibers were often damaged after compression of nerves in which nerve fibers at the core of the fascicle remained unaffected. The findings suggest that local external compression causes ischemia in nerve fibers served by transperineurial vessels, with severe compression causing axonal damage, while lesser degrees of compressive injury are associated with demyelination.

Pathology of experimental nerve compression

Peripheral nerve lesions are frequent occurrences in both human and animal patients, leading to important physiological and labor complications that affect the quality of life of those who suffer t...

https://www.tandfonline.com/doi/pdf/10.1080/2331205X.2018.1466404

Peripheral nerve injury and axonotmesis: State of the art and recent advances

Crush injury to the sciatic nerve causes oxidative stress. Alfa Lipoic acid (a-LA) is a neuroprotective metabolic antioxidant. This study was designed to investigate the antioxidant effects of pretreatment with a-LA on the crush injury of rat sciatic nerve. Forty rats were randomized into four groups. Group I and Group II received saline (2 ml, intraperitoneally) and a-LA (100 mg/kg, 2 ml, intraperitoneally) in the groups III and IV at the 24 and 1 hour prior to the crush injury. In groups II, III and IV, the left sciatic nerve was exposed and compressed for 60 seconds with a jeweler's forceps. In Group I (n = 10), the sciatic nerve was explored but not crushed. In all groups of rats, superoxide dismutase (SOD) and catalase (CAT) activities, as well as malondialdehyde (MDA) levels were measured in samples of sciatic nerve tissue. Compared to Group I, Group II had significantly decreased tissue SOD and CAT activities and elevated MDA levels indicating crush injury (p 0.05). A-LA administered before crush injury of the sciatic nerve showed significant protective effects against crush injury by decreasing the oxidative stress. A-LA should be considered in the treatment of peripheral nerve injuries, but further studies are needed to explain the mechanism of its neuroprotective effects.

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Intraperitoneal Alpha-Lipoic Acid to prevent neural damage after crush injury to the rat sciatic nerve.

STUDY DESIGN Oxidative/nitrosative stress in vertebral endplates of patients with low back pain and Modic changes (MCs) (types I, II, and III) endplate changes on magnetic resonance imaging. OBJECTIVE The aim of this study was to assess the levels of oxidative/nitrosative stress biomarkers in patients with MCs. SUMMARY OF BACKGROUND DATA Degenerated discs and endplate abnormalities is postulated as a possible source of low back pain. Oxidative/nitrosative stress plays an important the role in various human diseases. However, the presence of oxidative/nitrosative stress has not been studied in patients with low back pain and endplate changes on magnetic resonance imaging. METHODS Patients with MCI, II, and III (n = 32) and age- and sex-matched controls subjects (n = 15) were enrolled in this study. Also, 3-nitrotyrosine (3-NT) and nitric oxide levels as nitrosative stress biomarkers were measured with enzyme-linked immunosorbent assay. Also, the activities of catalase (CAT) and superoxide dismutase (SOD), and the levels of malondialdehyde (MDA) as oxidative stress biomarkers were determined on spectrophotometer. RESULTS Oxidative/nitrosative stress was confirmed by the significant elevation in nitric oxide, 3-NT, MDA and decreased of CAT and SOD activities in MCI compared with other MCs and the control group (P 0.05). However, the levels of oxidative stress biomarkers in patients with MCIII were slightly higher than that of the control group (P < 0.05). CONCLUSION Our findings indicated that oxidative/nitrosative stress in patients with MCI may be aggravated as a result of oxidant/antioxidant imbalance and it may cause formation of the lesion in these patients. However, the increased antioxidant activities and MDA, 3-NT levels in patients with MCII and MCIII may be an adaptative response to against oxidative/nitrosative stress. LEVEL OF EVIDENCE 4.

Oxidative/Nitrosative Stress in Patients With Modic Changes: Preliminary Controlled Study.

Achieving complete resolution of spinal hydatid cyst disease is quite challenging when bone is involved. Many authors reported the poor outcome of posterior decompression and laminectomy for intraosseous spinal hydatid disease. In an attempt to avoid a similar poor outcome, hydatid cysts were reached via both anterior and posterior surgical approaches in our patient. A 73-year-old man presented with complaints of low back and right leg pain. Symptoms or signs of systemic hydatid cyst disease were absent. MRI demonstrated a cystic lesion in the presacral/retroperitoneal region, involving the body of the sacrum and sacral canal. Computed tomography images showed enlargement of the sacral foraminae. The multiseptated cysts and their contents were isodense with cerebrospinal fluid. The cysts were removed via an anterior extraperitoneal approach, using a paramedian vertical incision, and then were also approached posteriorly via bilateral S1 hemilaminectomy. No neurological deficits occurred following surgery. The patient's symptoms completely disappeared after this combination of aggressive surgery and antihelminthic therapy. The application of both anterior and posterior approaches to intraosseous sacral hydatid cysts may be preferred when faced with hydatid disease in this location.

Combined anterior and posterior approach for sacral/retroperitoneal hydatid cyst disease: case report.

A 37-year-old Turkish woman with an intracranial lipoma of the quadrigeminal region is reported. Intracranial lipomas are extremely uncommon condition and generally occur in the midline areas, with an incidence of less than 0.1% of all intracranial tumours. Most lipomas were incidentally detected by autopsy or computed tomography (CT). The autopsy incidence of intracranial lipoma is 0.08% to 0.46%, while the incidence of CT finding is no more than 0.03% to 0.06%. Most intracranial lipomas are found incidentally during neuroradiological investigations. CT and MR examination usually lead to the diagnosis, because of the very low attenuation values of lipomas on CT and the short T1 and T2 on MR.We describe the findings of imaging studies, including computed tomography (CT), magnetic resonance (MR) imaging, along with a brief review of the literature.

https://print.ispub.com/api/0/ispub-article/6600

Idris Altun

Papers

Intraperitoneal Alpha-Lipoic Acid to prevent neural damage after crush injury to the rat sciatic nerve.

Oxidative/Nitrosative Stress in Patients With Modic Changes: Preliminary Controlled Study.

Combined anterior and posterior approach for sacral/retroperitoneal hydatid cyst disease: case report.

Lipoma of the Quadrigeminal Plate Cistern

G Protein-Coupled Estrogen Receptor Levels After Peripheral Nerve Injury in an Experimental Rat Model.