Autophagy as a protective mechanism in oxidative stress

Autophagy is the main catabolic process required for the removal of damaged organelles, aggregated proteins and intracellular pathogens from cells. Oxidative stress is accompanied by an increase in autophagy, which has a protective effect by maintaining the qualitative composition of mitochondria (mitophagy) and peroxisomes (pexophagy) followed by lysosomal degradation of organelles with high production of reactive oxygen species. Aggrephagy also removes toxic products formed during oxidative and carbonyl stress. Furthermore, autophagy can activate the antioxidant response element system and increase the expression of antioxidant enzyme genes. The protective role of autophagy can be useful in many pathological processes accompanied by the development of oxidative stress while at the same time it may cause chemoresistance, reducing the effectiveness of anti-tumor therapy.

Download Full-text

Effects of erdosteine on cyclosporin-A-induced nephrotoxicity

Human & Experimental Toxicology ◽

10.1177/0960327111417907 ◽

2011 ◽

Vol 31 (6) ◽

pp. 565-573 ◽

Cited By ~ 13

Author(s):

M Tutanc ◽

V Arica ◽

N Yılmaz ◽

A Nacar ◽

I Zararsiz ◽

...

Keyword(s):

Oxidative Stress ◽

Cyclosporin A ◽

Protective Role ◽

Control Group ◽

Albino Rats ◽

Protective Mechanism ◽

Antioxidant Parameters ◽

Group 2 ◽

Wistar Albino Rats

Aim: In cyclosporin-A (CsA)-induced toxicity, oxidative stress has been implicated as a potential responsible mechanism. Therefore, we aimed to investigate the protective role of erdosteine against CsA-induced nephrotoxicity in terms of tissue oxidant/antioxidant parameters and light microscopy in rats. Materials and methods: Wistar albino rats were randomly separated into four groups. Group 1 rats treated with sodium chloride served as the control, group 2 rats were treated with CsA, group 3 with CsA plus erdosteine, and group 4 with erdosteine alone. Animals were killed and blood samples were analyzed for blood urea nitrogen (BUN), serum creatinine (Cr), uric acid (UA), total protein (TP), and albumin (ALB) levels. Kidney sections were analyzed for malondialdehyde (MDA) and nitric oxide (NO) levels and superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) activities, as well as for histopathological changes. Results: In the CsA group, MDA, GSH-Px, BUN, and Cr levels were increased. The TP and ALB levels were decreased. These changes had been improved by erdosteine administration. Other biochemical parameters did not show any significant change. Conclusion: These results indicate that erdosteine produces a protective mechanism against CsA-induced nephrotoxicity and suggest a role of oxidative stress in pathogenesis.

Download Full-text

Protective Role of Perillic Acid Against Radiation−Induced Oxidative Stress, Cytokine Profile, DNA Damage, and Intestinal Toxicity in Mice

Journal of Environmental Pathology Toxicology and Oncology ◽

10.1615/jenvironpatholtoxicoloncol.v29.i3.40 ◽

2010 ◽

Vol 29 (3) ◽

pp. 199-212 ◽

Cited By ~ 11

Author(s):

P. Pratheeshkumar ◽

T.J. Raphael ◽

Girija Kuttan

Keyword(s):

Oxidative Stress ◽

Dna Damage ◽

Protective Role ◽

Cytokine Profile ◽

Intestinal Toxicity ◽

Radiation Induced

Download Full-text

Protective Role of Glutathione in the Hippocampus after Brain Ischemia

International Journal of Molecular Sciences ◽

10.3390/ijms22157765 ◽

2021 ◽

Vol 22 (15) ◽

pp. 7765

Author(s):

Youichirou Higashi ◽

Takaaki Aratake ◽

Takahiro Shimizu ◽

Shogo Shimizu ◽

Motoaki Saito

Keyword(s):

Oxidative Stress ◽

Neuronal Death ◽

Excitatory Amino Acid ◽

Ischemia Reperfusion ◽

Thiol Group ◽

Protective Role ◽

Key Factor ◽

Rate Limiting ◽

Cysteine Uptake

Stroke is a major cause of death worldwide, leading to serious disability. Post-ischemic injury, especially in the cerebral ischemia-prone hippocampus, is a serious problem, as it contributes to vascular dementia. Many studies have shown that in the hippocampus, ischemia/reperfusion induces neuronal death through oxidative stress and neuronal zinc (Zn2+) dyshomeostasis. Glutathione (GSH) plays an important role in protecting neurons against oxidative stress as a major intracellular antioxidant. In addition, the thiol group of GSH can function as a principal Zn2+ chelator for the maintenance of Zn2+ homeostasis in neurons. These lines of evidence suggest that neuronal GSH levels could be a key factor in post-stroke neuronal survival. In neurons, excitatory amino acid carrier 1 (EAAC1) is involved in the influx of cysteine, and intracellular cysteine is the rate-limiting substrate for the synthesis of GSH. Recently, several studies have indicated that cysteine uptake through EAAC1 suppresses ischemia-induced neuronal death via the promotion of hippocampal GSH synthesis in ischemic animal models. In this article, we aimed to review and describe the role of GSH in hippocampal neuroprotection after ischemia/reperfusion, focusing on EAAC1.

Download Full-text

Protective role of vitamin D against oxidative stress in diabetic retinopathy

Diabetes/Metabolism Research and Reviews ◽

10.1002/dmrr.3447 ◽

2021 ◽

Author(s):

Maria Stella Valle ◽

Cristina Russo ◽

Lucia Malaguarnera

Keyword(s):

Oxidative Stress ◽

Vitamin D ◽

Diabetic Retinopathy ◽

Protective Role

Download Full-text

Protective Role of Natural and Semi-Synthetic Tocopherols on TNFα-Induced ROS Production and ICAM-1 and Cl-2 Expression in HT29 Intestinal Epithelial Cells

Antioxidants ◽

10.3390/antiox10020160 ◽

2021 ◽

Vol 10 (2) ◽

pp. 160

Author(s):

Vladana Domazetovic ◽

Irene Falsetti ◽

Caterina Viglianisi ◽

Kristian Vasa ◽

Cinzia Aurilia ◽

...

Keyword(s):

Oxidative Stress ◽

Antioxidant Properties ◽

Intestinal Barrier ◽

Protective Role ◽

Intercellular Adhesion Molecule ◽

Intestinal Epithelial ◽

Intercellular Adhesion Molecule 1 ◽

Beneficial Effects ◽

Bowel Diseases

Vitamin E, a fat-soluble compound, possesses both antioxidant and non-antioxidant properties. In this study we evaluated, in intestinal HT29 cells, the role of natural tocopherols, α-Toc and δ-Toc, and two semi-synthetic derivatives, namely bis-δ-Toc sulfide (δ-Toc)2S and bis-δ-Toc disulfide (δ-Toc)2S2, on TNFα-induced oxidative stress, and intercellular adhesion molecule-1 (ICAM-1) and claudin-2 (Cl-2) expression. The role of tocopherols was compared to that of N-acetylcysteine (NAC), an antioxidant precursor of glutathione synthesis. The results show that all tocopherol containing derivatives used, prevented TNFα-induced oxidative stress and the increase of ICAM-1 and Cl-2 expression, and that (δ-Toc)2S and (δ-Toc)2S2 are more effective than δ-Toc and α-Toc. The beneficial effects demonstrated were due to tocopherol antioxidant properties, but suppression of TNFα-induced Cl-2 expression seems not only to be related with antioxidant ability. Indeed, while ICAM-1 expression is strongly related to the intracellular redox state, Cl-2 expression is TNFα-up-regulated by both redox and non-redox dependent mechanisms. Since ICAM-1 and Cl-2 increase intestinal bowel diseases, and cause excessive recruitment of immune cells and alteration of the intestinal barrier, natural and, above all, semi-synthetic tocopherols may have a potential role as a therapeutic support against intestinal chronic inflammation, in which TNFα represents an important proinflammatory mediator.

Download Full-text

Protective role of Sterculia tragacantha aqueous extract on pancreatic gene expression and oxidative stress parameters in streptozotocin-induced diabetic rats

Journal of Complementary and Integrative Medicine ◽

10.1515/jcim-2021-0020 ◽

2021 ◽

Vol 0 (0) ◽

Author(s):

Basiru Olaitan Ajiboye ◽

Babatunji Emmanuel Oyinloye ◽

Jennifer Chidera Awurum ◽

Sunday Amos Onikanni ◽

Adedotun Adefolalu ◽

...

Keyword(s):

Oxidative Stress ◽

Body Weight ◽

Protective Role ◽

Diabetic Rats ◽

Gene Expressions ◽

Ki 67 ◽

Oxidative Stress Parameters ◽

And Oxidative Stress ◽

Stress Parameters

Abstract Objectives The current study evaluates the protective role of aqueous extract of Sterculia tragacantha leaf (AESTL) on pancreatic gene expressions (insulin, PCNA, PDX-1, KI-67 and GLP-1R) and oxidative stress parameters in streptozotocin-induced diabetic rats. Methods Diabetes mellitus was induced into the experimental Wistar animals via intraperitoneal (IP) injection of streptozotocin (35 mg/kg body weight) and 5% glucose water was given to the rats for 24 h after induction. The animals were categorized into five groups of 10 rats each as follows normal control, diabetic control, diabetic rats administered AESTL (150 and 300 mg/kg body weight) and diabetic rats administered metformin (200 mg/kg) orally for two weeks. Thereafter, the animals were euthanized, blood sample collected, pancreas harvested and some pancreatic gene expressions (such as insulin, PCNA, PDX-1, KI-67, and GLP-1R)s as well as oxidative stress parameters were analyzed. Results The results revealed that AESTL significantly (p<0.05) reduced fasting blood glucose level, food and water intake, and lipid peroxidation in diabetic rats. Diabetic rats administered different doses of AESTL showed a substantial upsurge in body weight, antioxidant enzyme activities, and pancreatic gene expressions (insulin, PCNA, PDX-1, KI-67, and GLP-1R). Conclusions It can therefore be concluded that AESTL has the ability to protect the pancreas during diabetes mellitus conditions.

Download Full-text