scholarly journals Increased Oxidative Stress Response in Granulocytes from Older Patients with a Hip Fracture May Account for Slow Regeneration

2014 ◽  
Vol 2014 ◽  
pp. 1-9 ◽  
Author(s):  
Zhiyong Wang ◽  
Sabrina Ehnert ◽  
Christoph Ihle ◽  
Lilianna Schyschka ◽  
Stefan Pscherer ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Stress Response ◽  
Age Groups ◽  
Young Patients ◽  
The Elderly ◽  
Oxidative Stress Response ◽  
Proximal Femur Fracture ◽  
Mapk Activation ◽  
Stress Markers ◽  
Stress Response System

Proximal femur fracture, a typical fracture of the elderly, is often associated with morbidity, reduced quality of life, impaired physical function and increased mortality. There exists evidence that responses of the hematopoietic microenvironment to fractures change with age. Therefore, we investigated oxidative stress markers and oxidative stress-related MAPK activation in granulocytes from the young and the elderly with and without fractured long bones. Lipid peroxidation levels were increased in the elderly controls and patients. Aged granulocytes were more sensitive towards oxidative stress induced damage than young granulocytes. This might be due to the basally increased expression of SOD-1 in the elderly, which was not further induced by fractures, as observed in young patients. This might be caused by an altered MAPK activation. In aged granulocytes basal p38 and JNK activities were increased and basal ERK1/2 activity was decreased. Following fracture, JNK activity decreased, while ERK1/2 and p38 activities increased in both age groups. Control experiments with HL60 cells revealed that the observed p38 activation depends strongly on age. Summarizing, we observed age-dependent changes in the oxidative stress response system of granulocytes after fractures, for example, altered MAPK activation and SOD-1 expression. This makes aged granulocytes vulnerable to the stress stimuli of the fracture and following surgery.

The oxidative stress response system

2004 ◽  
pp. 59-76 ◽  
Author(s):  
André Korsloot ◽  
Cornelis A.M. van Gestel ◽  
Nico M. van Straalen
Keyword(s):  
Oxidative Stress ◽  
Stress Response ◽  
Oxidative Stress Response ◽  
Response System ◽  
Stress Response System

scholarly journals Oxidative Stress Parameters after Abdominal Hysterectomy and Their Relationships with Quality of Recovery

2019 ◽  
Vol 20 (2) ◽  
pp. 27-36 ◽  
Author(s):  
Danijela Jovanovic ◽  
Dragan R. Milovanovic ◽  
Nevena Jeremic ◽  
Tamara Nikolic ◽  
Isidora Stojic ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Stress Response ◽  
Smoking Status ◽  
Abdominal Hysterectomy ◽  
Oxidative Stress Response ◽  
Oxidative Stress Markers ◽  
Quality Of Recovery ◽  
Stress Markers ◽  
Duration Of Surgery

Abstract Study aimed to investigate relationship between oxidative stress markers and postoperative recovery in woman after abdominal hysterectomy, as well as to test the hypothesis that different analgesics differently influence redox status. The quality of recovery was evaluated with a QoR-40 questionnaire in fifty-one patients who underwent abdominal hysterectomy, preoperatively and on the 1st, 2nd, 3rd postoperative days (POD1,2,3). Blood samples were collected at baseline (T0), 3 (T1), 24 (T2), 48 (T3) and 72 (T4) hours after surgery. Oxidative stress markers concentrations (TBARS, NO2−, H2O2, O2− ) as well as antioxidative enzymes (SOD, CAT, and GSH) were analyzed. QoR-40 total score significantly declined on POD1 and POD2 and returned to baseline levels on POD3 (p<0.001). H2O2 levels significantly decreased from T0 to T3 and then, increased at T4 (p=0,011). Changes of TBARS and H2O2 from T0 to T3 showed significant and negative correlation (r=−0.303, p=0.046). There was no significant correlation between QoR-40 total score and any parameter of oxidative stress response (p>0.05). Changes in TBARS levels from T0 to T3 were statistically significant between the study subgroups primarily due to increase of the concentrations in patients receiving paracetamol (p=0.031). Patients age, duration of surgery and cigarette smoking status showed significant influcences on and association with some oxidative stress response markers (TBARS, O2−, CAT) (p<0.05). Women who underwent hysterectomy had significant changes of H2O2 and TBARS activity however, those changes were not associated with changes of QoR-40 total scores during recovery.

scholarly journals Targeting the Oxidative Stress Response System of Fungi with Redox-Potent Chemosensitizing Agents

2012 ◽  
Vol 3 ◽  
Author(s):  
Jong H. Kim ◽  
Kathleen L. Chan ◽  
Natália C. G. Faria ◽  
M. de L. Martins ◽  
Bruce C. Campbell
Keyword(s):  
Oxidative Stress ◽  
Stress Response ◽  
Oxidative Stress Response ◽  
Response System ◽  
Stress Response System

scholarly journals Differential oxidative stress response in young children and the elderly following exposure to PM2.5

2008 ◽  
Vol 14 (1) ◽  
pp. 60-66 ◽  
Author(s):  
Kyoungwoo Kim ◽  
Eun-Young Park ◽  
Kwan-Hee Lee ◽  
Jung-Duck Park ◽  
Yong-Dae Kim ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Stress Response ◽  
Young Children ◽  
The Elderly ◽  
Oxidative Stress Response

scholarly journals Physiopathological Bases of the Disease Caused by HACE1 Mutations: Alterations in Autophagy, Mitophagy and Oxidative Stress Response

2020 ◽  
Vol 9 (4) ◽  
pp. 913
Author(s):  
Olatz Ugarteburu ◽  
Marta Sánchez-Vilés ◽  
Julio Ramos ◽  
Tamara Barcos-Rodríguez ◽  
Gloria Garrabou ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Stress Response ◽  
Oxidative Damage ◽  
Neurodevelopmental Disorder ◽  
Psychomotor Retardation ◽  
Oxidative Stress Response ◽  
Autophagic Flux ◽  
Mrna Levels ◽  
Mitochondrial Oxidative Stress ◽  
Stress Markers

Recessive HACE1 mutations are associated with a severe neurodevelopmental disorder (OMIM: 616756). However, the physiopathologycal bases of the disease are yet to be completely clarified. Whole-exome sequencing identified homozygous HACE1 mutations (c.240C>A, p.Cys80Ter) in a patient with brain atrophy, psychomotor retardation and 3-methylglutaconic aciduria, a biomarker of mitochondrial dysfunction. To elucidate the pathomechanisms underlying HACE1 deficiency, a comprehensive molecular analysis was performed in patient fibroblasts. Western Blot demonstrated the deleterious effect of the mutation, as the complete absence of HACE1 protein was observed. Immunofluorescence studies showed an increased number of LC3 puncta together with the normal initiation of the autophagic cascade, indicating a reduction in the autophagic flux. Oxidative stress response was also impaired in HACE1 fibroblasts, as shown by the reduced NQO1 and Hmox1 mRNA levels observed in H2O2-treated cells. High levels of lipid peroxidation, consistent with accumulated oxidative damage, were also detected. Although the patient phenotype could resemble a mitochondrial defect, the analysis of the mitochondrial function showed no major abnormalities. However, an important increase in mitochondrial oxidative stress markers and a strong reduction in the mitophagic flux were observed, suggesting that the recycling of damaged mitochondria might be targeted in HACE1 cells. In summary, we demonstrate for the first time that the impairment of autophagy, mitophagy and oxidative damage response might be involved in the pathogenesis of HACE1 deficiency.

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