Anti-steroidogenic effects of cholesterol hydroperoxide trafficking in MA-10 Leydig cells: Role of mitochondrial lipid peroxidation and inhibition thereof by selenoperoxidase GPx4

2022 ◽  
Author(s):  
Pawel Pabisz ◽  
Jerzy Bazak ◽  
Albert W. Girotti ◽  
Witold Korytowski
Keyword(s):  
Lipid Peroxidation ◽  
Leydig Cells ◽  
Mitochondrial Lipid ◽  
Cholesterol Hydroperoxide

scholarly journals Melatonin Inhibits Benzene-Induced Lipid Peroxidation in Rat Liver

2010 ◽  
Vol 61 (1) ◽  
pp. 11-18 ◽  
Author(s):  
Seema Sharma ◽  
Suresh Rana
Keyword(s):  
Lipid Peroxidation ◽  
Single Dose ◽  
Rat Liver ◽  
Treated Group ◽  
Melatonin Treatment ◽  
Liver Histopathology ◽  
Microsomal Lipid Peroxidation ◽  
Significant Difference ◽  
Mitochondrial Lipid

Melatonin Inhibits Benzene-Induced Lipid Peroxidation in Rat LiverWe studied the antioxidative role of melatonin against benzene toxicity in rat liver. The inhibition of mitochondrial and microsomal lipid peroxidation differed between 24-hour (single-dose), 15-day, and 30-day treatments. Inhibition of mitochondrial lipid peroxidation was the highest after the single dose of melatonin, whereas highest microsomal inhibition was recorded after 30 days of melatonin treatment. No significant difference was recorded between 15-day and 30-day treatments. Cytochrome P 4502E1 (CYP 4502E1) activity declined after the single-dose and 15-day melatonin treatment in the benzene-treated group, but it rose again, though not significantly after 30 days of treatment. Liver histopathology generally supported these findings. Phenol concentration in the urine samples declined in melatonin and benzene-treated rats. Our results show that melatonin affects CYP 4502E1, which is responsible for benzene metabolism. Inhibition of its metabolism correlated with lower lipid peroxidation. In conclusion, melatonin was found to be protective against lipid peroxidation induced by benzene.

Role of monoamine oxidase in the intensification of mitochondrial lipid peroxidation in experimental myocardial necrosis

1988 ◽  
Vol 106 (1) ◽  
pp. 965-967
Author(s):  
A. I. Dzhafarov ◽  
N. M. Magomedov ◽  
A. M. Azimova ◽  
N. I. Alieva ◽  
D. N. Dagkesamanskaya
Keyword(s):  
Lipid Peroxidation ◽  
Monoamine Oxidase ◽  
Myocardial Necrosis ◽  
Mitochondrial Lipid

Role of dyslipidaemia and lipid peroxidation in pregnancy induced hypertension

2015 ◽  
Vol 4 (3) ◽  
pp. 205 ◽  
Author(s):  
Shikha Saxena ◽  
KV Thimmaraju ◽  
PremC Srivastava ◽  
AyazK Mallick ◽  
Biswajit Das ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Pregnancy Induced Hypertension ◽  
Induced Hypertension ◽  
In Pregnancy

On the role of lipid metabolism and lipid peroxidation in the development of retinal disorders in type 2 diabetic rats with myopia

2019 ◽  
Vol 82 (5) ◽  
pp. 56-63
Author(s):  
Abdulhadi Mohammad ◽  
◽  
I. Mikheitseva ◽  
S. Kolomiichuk ◽  
◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Lipid Metabolism ◽  
Diabetic Rats ◽  
Retinal Disorders ◽  
Type 2 Diabetic

scholarly journals Insights in the Role of Lipids, Oxidative Stress and Inflammation in Rheumatoid Arthritis Unveiled by New Trends in Lipidomic Investigations

Antioxidants ◽  
2021 ◽  
Vol 10 (1) ◽  
pp. 45
Author(s):  
Helena Beatriz Ferreira ◽  
Tânia Melo ◽  
Artur Paiva ◽  
Maria do Rosário Domingues
Keyword(s):  
Rheumatoid Arthritis ◽  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Lipid Profile ◽  
Inflammatory Responses ◽  
Molecular Level ◽  
Lipid Hydroperoxides ◽  
Lipid Species ◽  
Inflammatory Autoimmune Disease

Rheumatoid arthritis (RA) is a highly debilitating chronic inflammatory autoimmune disease most prevalent in women. The true etiology of this disease is complex, multifactorial, and is yet to be completely elucidated. However, oxidative stress and lipid peroxidation are associated with the development and pathogenesis of RA. In this case, oxidative damage biomarkers have been found to be significantly higher in RA patients, associated with the oxidation of biomolecules and the stimulation of inflammatory responses. Lipid peroxidation is one of the major consequences of oxidative stress, with the formation of deleterious lipid hydroperoxides and electrophilic reactive lipid species. Additionally, changes in the lipoprotein profile seem to be common in RA, contributing to cardiovascular diseases and a chronic inflammatory environment. Nevertheless, changes in the lipid profile at a molecular level in RA are still poorly understood. Therefore, the goal of this review was to gather all the information regarding lipid alterations in RA analyzed by mass spectrometry. Studies on the variation of lipid profile in RA using lipidomics showed that fatty acid and phospholipid metabolisms, especially in phosphatidylcholine and phosphatidylethanolamine, are affected in this disease. These promising results could lead to the discovery of new diagnostic lipid biomarkers for early diagnosis of RA and targets for personalized medicine.

Ferroptosis and cardiovascular disease: role of free radical-induced lipid peroxidation

2021 ◽  
pp. 1-11
Author(s):  
Xin Chen ◽  
Xuan Li ◽  
Xiaodong Xu ◽  
Luxiao Li ◽  
Ningning Liang ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Lipid Peroxidation ◽  
Free Radical

Modulation of collagen synthesis by growth factors: The role of ascorbate-stimulated lipid peroxidation

1991 ◽  
Vol 289 (1) ◽  
pp. 6-11 ◽  
Author(s):  
Jeffrey C. Geesin ◽  
Laura J. Hendricks ◽  
Joel S. Gordon ◽  
Richard A. Berg
Keyword(s):  
Lipid Peroxidation ◽  
Growth Factors ◽  
Collagen Synthesis

scholarly journals Silencing of MEG3 attenuated the role of lipopolysaccharides by modulating the miR-93-5p/PTEN pathway in Leydig cells

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Xu Zhou ◽  
Jingliang He ◽  
Jinbo Chen ◽  
Yu Cui ◽  
Zhenyu Ou ◽  
...  
Keyword(s):  
Cell Viability ◽  
Cell Apoptosis ◽  
Leydig Cells ◽  
Treatment Strategies ◽  
Pten Expression ◽  
Luciferase Reporter ◽  
Western Blots ◽  
New Treatment ◽  
Lps Treatment

Abstract Background Leydig cells reflect the activation of inflammation, decrease of androgen production, inhibition of cell growth and promotion of cell apoptosis under orchitis. Maternally expressed gene 3 (MEG3) exerts a crucial role in various human diseases, but under orchitis, the role and underlying molecular mechanism of MEG3 in Leydig cells remain unclear. Methods Lipofectamine 2000 was used for the cell transfections. qPCR and western blots assay were applied to assess the gene expression. ELISA assay was used to measure the TNFα, IL6 and testosterone secretion. CCK8 and EdU assay was employ to test the cell viability and proliferation respectively. Luciferase reporter and RIP assay were introduced to detect the binding of miR-93-5p with MEG3 and PTEN. Results Lipopolysaccharides (LPS) induced TNFα and IL6 secretion, lowered testosterone production, inhibited cell viability and proliferation, and induced cell apoptosis in Leydig cells. MEG3 was upregulated in Leydig cells treated with LPS and that knockdown of MEG3 inhibited the role of LPS in Leydig cells. MEG3 absorbed miR-93-5p and that suppression of miR-93-5p restored the role of silenced MEG3 in Leydig cells under LPS treatment. miR-93-5p inhibited PTEN expression and that over-expressed PTEN alleviated the effect of miR-93-5p in Leydig cells treated with LPS. LPS activated the MEG3/miR-93-5p/PTEN signalling pathway in Leydig cells. Conclusions This study revealed that MEG3 serves as a molecular sponge to absorb miR-93-5p, thus leading to elevation of PTEN expression in Leydig cells under LPS treatment, offering a theoretical basis on which to establish potential new treatment strategies for orchitis.

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