Antioxidant defense of fish collagen peptides attenuates oxidative stress in gastric mucosa of experimentally ulcer-induced rats

Author(s):  
Divya K. Vijayan ◽  
P. R. Sreerekha ◽  
Pavan Kumar Dara ◽  
B. Ganesan ◽  
Suseela Mathew ◽  
...  
2020 ◽  
Vol 245 (14) ◽  
pp. 1260-1267
Author(s):  
Sylwia Dzięgielewska-Gęsiak ◽  
Dorota Stołtny ◽  
Alicja Brożek ◽  
Małgorzata Muc-Wierzgoń ◽  
Ewa Wysocka

Insulin resistance (IR) may be associated with oxidative stress and leads to cardiovascular disorders. Current research focuses on interplay between insulin-resistance indices and oxidant-antioxidant markers in elderly individuals with or without insulin-resistance. The assessment involved anthropometric data (weight, height, BMI, percentage of body fat (FAT)) and biochemical tests (glucose, lipids, serum insulin and plasma oxidant-antioxidant markers: Thiobarbituric Acid-Reacting Substances (TBARS), Cu,Zn-superoxide dismutase (SOD-1) and total antioxidant status). Insulin resistance index (IR) assuming a cut-off point of 0.3 allows to divides groups into: insulin sensitive group (InsS) IR < 0,3 ( n = 35, median age 69.0 years) and insulin-resistant group (InsR) IR ≥ 0.3 ( n = 51, median age 71.0 years). Lipids and antioxidant defense system markers did not differentiate the investigated groups. In the InsR elderly group, the FAT was increased ( P < 0.000003) and TBARS ( P = 0.008) concentration decreased in comparison with InsS group. A positive correlation for SOD-1 and total antioxidant status ( P < 0.05; r =  0.434) and a negative correlation for TBARS and age ( P < 0.05 with r = −0.421) were calculated in InsR individuals. In elderly individuals, oxidative stress persists irrespective of insulin-resistance status. We suggest that increased oxidative stress may be consequence of old age. An insulin action identifies those at high risk for atherosclerosis, via congruent associations with oxidative stress and extra- and intra-cellular antioxidant defense systems. Thus, we maintain that insulin-resistance is not the cause of aging. Impact statement Insulin resistance is associated with oxidative stress leading to cardiovascular diseases. However, little research has been performed examining elderly individuals with or without insulin-resistance. We demonstrate that antioxidant defense systems alone is not able to abrogate insulin action in elderly individuals at high risk for atherosclerosis, whereas the combined oxidant-antioxidant markers (thiobarbituric acid-reacting substances (TBARS), Cu,Zn-superoxide dismutase (SOD-1), and total antioxidant status (TAS)) might be more efficient and perhaps produce better clinical outcome. In fact, a decrease in oxidative stress and strong interaction between antioxidant defense can be seen only among insulin-resistant elderly individuals. This is, in our opinion, valuable information for clinicians, since insulin-resistance is considered strong cardiovascular risk factor.


2004 ◽  
Vol 68 (10) ◽  
pp. 1939-1946 ◽  
Author(s):  
Andrea J. Moreira ◽  
Christina Fraga ◽  
María Alonso ◽  
Pilar S. Collado ◽  
Claudio Zetller ◽  
...  

2013 ◽  
Vol 304 (5) ◽  
pp. E495-E506 ◽  
Author(s):  
S. Keipert ◽  
M. Ost ◽  
A. Chadt ◽  
A. Voigt ◽  
V. Ayala ◽  
...  

Ectopic expression of uncoupling protein 1 (UCP1) in skeletal muscle (SM) mitochondria increases lifespan considerably in high-fat diet-fed UCP1 Tg mice compared with wild types (WT). To clarify the underlying mechanisms, we investigated substrate metabolism as well as oxidative stress damage and antioxidant defense in SM of low-fat- and high-fat-fed mice. Tg mice showed an increased protein expression of phosphorylated AMP-activated protein kinase, markers of lipid turnover (p-ACC, FAT/CD36), and an increased SM ex vivo fatty acid oxidation. Surprisingly, UCP1 Tg mice showed elevated lipid peroxidative protein modifications with no changes in glycoxidation or direct protein oxidation. This was paralleled by an induction of catalase and superoxide dismutase activity, an increased redox signaling (MAPK signaling pathway), and increased expression of stress-protective heat shock protein 25. We conclude that increased skeletal muscle mitochondrial uncoupling in vivo does not reduce the oxidative stress status in the muscle cell. Moreover, it increases lipid metabolism and reactive lipid-derived carbonyls. This stress induction in turn increases the endogenous antioxidant defense system and redox signaling. Altogether, our data argue for an adaptive role of reactive species as essential signaling molecules for health and longevity.


2009 ◽  
Vol 39 (4) ◽  
pp. 723-730 ◽  
Author(s):  
Jihong Qin ◽  
Qing Liu

In the subalpine zone of the Qinghai–Tibetan Plateau of China, Dragon spruce (Picea asperata Mast.) is commonly used for reforestation. The aim of the present work was to study the effects of seasonally frozen soil on the germination of P. asperata seeds and to investigate whether these effects were associated with resumption of the antioxidant defense system. The nonfrozen treatment resulted in near failure of germination (1%) and was associated with relatively high levels of hydrogen peroxide (H2O2) and low activities of superoxide dismutase (SOD), catalase (CAT), and ascorbate peroxide (APX). Germination of P. asperata seeds at 10 cm under the seasonally frozen soil was higher than that at 5 cm by 26%; this higher germination rate was associated with the recovery of SOD, CAT, and APX activities. The levels of malondialdehyde (MDA) in seeds from seasonally frozen treatments were higher than those in the nonfrozen treatment, implying greater lipid peroxidation and that frozen seeds might have suffered from oxidative stress. The results indicate that seasonally frozen soil facilitated the germination of P. asperata seeds and that germination was closely related to the resumption of antioxidant enzymes activity. Overall, these findings suggest that the disappearance of seasonally frozen ground caused by global warming might result in failure of regeneration of P. asperata.


2001 ◽  
Vol 96 (6) ◽  
pp. 1758-1766 ◽  
Author(s):  
Brigitte Pignatelli ◽  
Brigitte Bancel ◽  
Martin Plummer ◽  
Shinya Toyokuni ◽  
Louis-Marc Patricot ◽  
...  

Chemosphere ◽  
2022 ◽  
Vol 287 ◽  
pp. 131911
Author(s):  
Doyel Roy ◽  
Sinchan Adhikari ◽  
Ayan Adhikari ◽  
Supriya Ghosh ◽  
Ikbal Azahar ◽  
...  

Cancers ◽  
2021 ◽  
Vol 13 (5) ◽  
pp. 1138
Author(s):  
Martina Schiavello ◽  
Elena Gazzano ◽  
Loredana Bergandi ◽  
Francesca Silvagno ◽  
Roberta Libener ◽  
...  

Although asbestos has been banned in most countries around the world, malignant pleural mesothelioma (MPM) is a current problem. MPM is an aggressive tumor with a poor prognosis, so it is crucial to identify new markers in the preventive field. Asbestos exposure induces oxidative stress and its carcinogenesis has been linked to a strong oxidative damage, event counteracted by antioxidant systems at the pulmonary level. The present study has been focused on some redox-sensitive transcription factors that regulate cellular antioxidant defense and are overexpressed in many tumors, such as Nrf2 (Nuclear factor erythroid 2-related factor 2), Ref-1 (Redox effector factor 1), and FOXM1 (Forkhead box protein M1). The research was performed in human mesothelial and MPM cells. Our results have clearly demonstrated an overexpression of Nrf2, Ref-1, and FOXM1 in mesothelioma towards mesothelium, and a consequent activation of downstream genes controlled by these factors, which in turn regulates antioxidant defense. This event is mediated by oxidative free radicals produced when mesothelial cells are exposed to asbestos fibers. We observed an increased expression of Nrf2, Ref-1, and FOXM1 towards untreated cells, confirming asbestos as the mediator of oxidative stress evoked at the mesothelium level. These factors can therefore be considered predictive biomarkers of MPM and potential pharmacological targets in the treatment of this aggressive cancer.


2006 ◽  
Vol 290 (5) ◽  
pp. G847-G851 ◽  
Author(s):  
Jinah Choi ◽  
J.-H. James Ou

Hepatitis C virus (HCV) is a major cause of viral hepatitis that can progress to hepatic fibrosis, steatosis, hepatocellular carcinoma, and liver failure. HCV infection is characterized by a systemic oxidative stress that is most likely caused by a combination of chronic inflammation, iron overload, liver damage, and proteins encoded by HCV. The increased generation of reactive oxygen and nitrogen species, together with the decreased antioxidant defense, promotes the development and progression of hepatic and extrahepatic complications of HCV infection. This review discusses the possible mechanisms of HCV-induced oxidative stress and its role in HCV pathogenesis.


Sign in / Sign up

Export Citation Format

Share Document