Antioxidant enzymes, occupational stress and burnout in workers of a prehospitalary emergency service

Moragón, Ángela Casado; García, N. de Lucas; Fernández, Manuel; Rodriguez-Manzaneque, Alberto Sánchez; Fraile, José A Jimenez

doi:10.1097/00063110-200506000-00003

Cited by 23 publications

(16 citation statements)

References 11 publications

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“…[28][29][30][31][32][33] The present results demonstrate that the absence of testosterone leads to decreased antioxidant status, thus promoting oxidative stress as suggested previously. 17 Drinking grapefruit juice prevented the decrease in plasma antioxidant capacity in ORX rats, while it numerically enhanced antioxidant status of the sham-control rats by 1.6%.…”

Section: Discussionsupporting

confidence: 74%

Grapefruit Juice Modulates Bone Quality in Rats

Deyhim

Mandadi²,

Faraji³

et al. 2008

Journal of Medicinal Food

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Hypogonadism and oxidative stress increase the risk for developing osteoporosis. The objective of this research was to evaluate the efficacy of drinking grapefruit juice on bone quality in orchidectomized (ORX) and non-ORX rats. Fifty-six 90-day-old male Sprague-Dawley rats were equally divided into four groups--non-ORX rats (sham), sham + grapefruit juice, ORX, and ORX + grapefruit juice--and treated for 60 days. Thereafter, all rats were sacrificed to determine the plasma antioxidant status, insulin-like growth factor I (IGF-I), and indices of bone turnover, bone quality, and calcium and magnesium concentrations in the bone, urine, and feces. Orchidectomy decreased (P < .05) antioxidant status, bone quality, and bone mineral contents and increased (P < .05) indices of bone turnover, urinary deoxypridinoline, calcium, and magnesium, and fecal calcium excretions. In contrast to the ORX group, ORX rats that drank grapefruit juice had an increase (P < .05) in antioxidant status, bone density, and bone mineral contents, delayed femoral fracture, and slowed down (P < .05) bone turnover rate and tended to have a decrease (P = .08) in urinary deoxypridinoline. In sham-treated animals, drinking grapefruit juice increased (P < .05) bone density and tended to increase the femoral strength. The concentration of IGF-I in the plasma was not affected across treatments. In conclusion, drinking grapefruit juice positively affected bone quality by enhancing bone mineral deposition in ORX rats and by improving bone density in non-ORX rats via an undefined mechanism.

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Section: Discussionsupporting

confidence: 74%

Grapefruit Juice Modulates Bone Quality in Rats

Deyhim

Mandadi²,

Faraji³

et al. 2008

Journal of Medicinal Food

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“…ROS are formed in the human body in the cytosol, mitochondria, lysosomes, peroxisomes, and plasma membranes under both physiological and pathological conditions [20]; their levels can increase by stress situations such as occupational stress [21,22]. …”

Section: Discussionmentioning

confidence: 99%

Oxidative Stress Induced by Lipid Peroxidation Is Related with Inflammation of Demyelination and Neurodegeneration in Multiple Sclerosis

et al. 2014

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Background: Multiple sclerosis (MS) is a chronic autoimmune demyelination disorder of the central nervous system (CNS) and its etiology remains unknown. The inflammatory environment in demyelinating lesions leads to the generation of oxygen- and nitrogen-free radicals as well as proinflammatory cytokines, which contribute to the development and progression of multiple sclerosis. Inflammation can lead to oxidative stress and vice versa. Thus, oxidative stress is involved in the inflammation leading demyelination and neurodegeneration in the pathogenesis of multiple sclerosis. Summary: The present study aims to determine two biochemical markers of oxidative stress: TAC and MDA and to show their correlations whether oxidative stress reaction occurs in the demyelination through analyzing samples including peripheral blood and cerebrospinal fluid (CSF) from patients with relapsing-remitting MS (RR-MS). Totally, there were 20 patients in the control groups made from individuals with normal pressure hydrocephalus. Thirty MS patients diagnosed with McDonald diagnostic criteria (2010) treated with methylprednisolone were included in this study. Data were stratified by the degree of severity in order to clarify the role of oxidative stress in the mechanisms of MS and to assess its potential as a biomarker. Thirty clinically definite RRMS patients were enrolled in this study. Levels of MDA, GSH, total antioxidant capacity TAC, GSH-Px and ROS, were determined in serum of the control group and RRMS patients in 7 days before MP (methylprednisolone) treatment and one month after MP treatment. Statistical analysis was performed with one-way analysis of variance (ANOVA), followed by LSD's post hoc tests. Key Messages: Oxidative stress precedes the inflammatory response in the multiple sclerosis patients. And methylprednisolone treatment can decrease brain antioxidant enzymes to reduce the neuroinflammatory attack.

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“…The cytosolic fractions, thus obtained, were used for enzyme activities. Catalase activity was assayed (Moragon et al, 2005). The reaction mixture contained sodium phosphate buffer (0.05 M, pH 7.0), 50 mM Ϫ1 H 2 O 2 , and 50 l of enzyme extract in a 3-ml volume.…”

Section: Liposomal Flavonoid Protects Arsenite-induced Liver Fibrosismentioning

confidence: 99%

Hepatoprotective Activity of Liposomal Flavonoid against Arsenite-Induced Liver Fibrosis

Mandal¹,

Das²,

Basu³

et al. 2006

J Pharmacol Exp Ther

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Arsenic, the environmental metalloid toxicant, is known to induce oxidative damage to liver and produce hepatic fibrosis. The theme of our study was to optimize and evaluate the therapeutic efficacy of galactosylated liposomal flavonoidal antioxidant, quercetin (QC), in combating arsenic-induced hepatic fibrogenesis. The rats of the hepatic damage group were injected s.c. a single dose of sodium arsenite (NaAsO 2 ) (100.06 M/kg b. wt. in 0.5 ml of physiological saline). Hepatocytes and stellate cells were separated. Mitochondrial membranes were isolated from all those separated cells. Oxidative damage was monitored at different isolated subcellular parts of different hepatic cells. Liver fibrosis was also induced by the injection of NaAsO 2 . Galactosylated liposomal QC injection before NaAsO 2 treatment checked fibrogenesis completely by protecting the liver from oxidative attack in cellular and subcellular levels. The maximal protections from hepatocellular and fatty metamorphosis, necrosis, Kupffer cell hyperplasia, fibrosis, and in the deposition of collagen contents were observed and reconfirmed by our histopathological and histochemical analysis when rats were treated with galactosylated liposomal QC before NaAsO 2 injection. Application of galactosylated liposomal QC may be a potent therapeutic approach for NaAsO 2 -induced fibrogenesis through a complete protection against oxidative attack in cellular and subcellular parts of rat liver.

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Antioxidant enzymes, occupational stress and burnout in workers of a prehospitalary emergency service

Cited by 23 publications

References 11 publications

Grapefruit Juice Modulates Bone Quality in Rats

Grapefruit Juice Modulates Bone Quality in Rats

Oxidative Stress Induced by Lipid Peroxidation Is Related with Inflammation of Demyelination and Neurodegeneration in Multiple Sclerosis

Hepatoprotective Activity of Liposomal Flavonoid against Arsenite-Induced Liver Fibrosis

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