p62/SQSTM1 protects against cisplatin-induced oxidative stress in kidneys by mediating the cross talk between autophagy and the Keap1-Nrf2 signalling pathway

Premature ovarian failure (POF) is a common cause of infertility in premenopausal women who are unavoidably exposed to cytotoxic therapy. Radiotherapy is one of the most effective cytotoxic treatments. However, the radiosensitivity of ovarian tissues limits its therapeutic outcome and results in the depletion of the primordial follicle and loss of fertility. Therefore, the need for an effective radioprotective therapy is evident especially when none of the current clinically used modalities for radioprotection succeeds efficiently. The present study investigated the potential radioprotective effect of carvacrol (CAR) (80 mg) or thymol (80 mg) on gamma- (γ-) irradiation-induced ovarian damage as well as their role in the cross-talk between IGF-1 and TNF-α signaling and antioxidative activity. In immature female Wister rats, a single dose of whole-body irradiation (3.2 Gy, L D 20 ) produced considerable ovarian damage, which was evident by histopathological findings and hormonal changes. Interestingly, pretreatment with CAR or thymol significantly enhanced the follicular development and restored the anti-Mullerian hormone (AMH), E2, and FSH levels. Both essential oils improved the irradiation-mediated oxidative stress and reduction in proliferating cell nuclear antigen (PCNA) expression. Moreover, irradiated rats exhibited an inverse relationship between IGF-1 and TNF-α levels two days post irradiation, which was further inverted by the pretreatment with CAR and thymol and ought to contribute in their radioprotective mechanisms. In conclusion, CAR and thymol showed a radioprotective effect and rescued the ovarian reserve mainly through counteracting oxidative stress and the dysregulated cross-talk between IGF-1 and TNF-α.

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Unravelling the cross-talk between iron starvation and oxidative stress responses highlights the key role of PerR (alr0957) in peroxide signalling in the cyanobacteriumNostoc PCC 7120

Environmental Microbiology Reports ◽

10.1111/1758-2229.12157 ◽

2014 ◽

Vol 6 (5) ◽

pp. 468-475 ◽

Cited By ~ 21

Author(s):

Fan Yingping ◽

Sylvain Lemeille ◽

Emmanuel Talla ◽

Annick Janicki ◽

Yann Denis ◽

...

Keyword(s):

Oxidative Stress ◽

Cross Talk ◽

Stress Responses ◽

Iron Starvation ◽

The Cross ◽

Pcc 7120 ◽

Oxidative Stress Responses ◽

And Oxidative Stress

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The cross-talk between oxidative stress and endocannabinoid system in keratinocytes after UV irradiation

Free Radical Biology and Medicine ◽

10.1016/j.freeradbiomed.2015.07.102 ◽

2015 ◽

Vol 86 ◽

pp. S28

Author(s):

Agnieszka Gęgotek ◽

Wojciech Luczaj ◽

Ewa Ambrozewicz ◽

Katarzyna Bielawska ◽

Elzbieta Skrzydlewska

Keyword(s):

Oxidative Stress ◽

Uv Irradiation ◽

Cross Talk ◽

Endocannabinoid System ◽

The Cross

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Cross-Talk between Mitochondrial Dysfunction-Provoked Oxidative Stress and Aberrant Noncoding RNA Expression in the Pathogenesis and Pathophysiology of SLE

International Journal of Molecular Sciences ◽

10.3390/ijms20205183 ◽

2019 ◽

Vol 20 (20) ◽

pp. 5183 ◽

Cited By ~ 2

Author(s):

Chang-Youh Tsai ◽

Song-Chou Hsieh ◽

Cheng-Shiun Lu ◽

Tsai-Hung Wu ◽

Hsien-Tzung Liao ◽

...

Keyword(s):

Oxidative Stress ◽

Mitochondrial Dysfunction ◽

Cross Talk ◽

Noncoding Rna ◽

Nitrosative Stress ◽

Noncoding Rnas ◽

The Body ◽

Rna Expression ◽

Epigenetic Regulations ◽

The Cross

Systemic lupus erythematosus (SLE) is a prototype of systemic autoimmune disease involving almost every organ. Polygenic predisposition and complicated epigenetic regulations are the upstream factors to elicit its development. Mitochondrial dysfunction-provoked oxidative stress may also play a crucial role in it. Classical epigenetic regulations of gene expression may include DNA methylation/acetylation and histone modification. Recent investigations have revealed that intracellular and extracellular (exosomal) noncoding RNAs (ncRNAs), including microRNAs (miRs), and long noncoding RNAs (lncRNAs), are the key molecules for post-transcriptional regulation of messenger (m)RNA expression. Oxidative and nitrosative stresses originating from mitochondrial dysfunctions could become the pathological biosignatures for increased cell apoptosis/necrosis, nonhyperglycemic metabolic syndrome, multiple neoantigen formation, and immune dysregulation in patients with SLE. Recently, many authors noted that the cross-talk between oxidative stress and ncRNAs can trigger and perpetuate autoimmune reactions in patients with SLE. Intracellular interactions between miR and lncRNAs as well as extracellular exosomal ncRNA communication to and fro between remote cells/tissues via plasma or other body fluids also occur in the body. The urinary exosomal ncRNAs can now represent biosignatures for lupus nephritis. Herein, we’ll briefly review and discuss the cross-talk between excessive oxidative/nitrosative stress induced by mitochondrial dysfunction in tissues/cells and ncRNAs, as well as the prospect of antioxidant therapy in patients with SLE.

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