p,p′-Dichlorodiphenoxydichloroethylene induced apoptosis of Sertoli cells through oxidative stress-mediated p38 MAPK and mitochondrial pathway

2011 ◽  
Vol 202 (1) ◽  
pp. 55-60 ◽  
Author(s):  
Yang Song ◽  
Yuqin Shi ◽  
Haige Yu ◽  
Yafei Hu ◽  
Yinan Wang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
P38 Mapk ◽  
Sertoli Cells ◽  
Mitochondrial Pathway ◽  
Induced Apoptosis

scholarly journals The REDD1/TXNIP Complex Accelerates Oxidative Stress-Induced Apoptosis of Nucleus Pulposus Cells through the Mitochondrial Pathway

2021 ◽  
Vol 2021 ◽  
pp. 1-22
Author(s):  
Huipeng Yin ◽  
Kun Wang ◽  
Abhirup Das ◽  
Gaocai Li ◽  
Yu Song ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Intervertebral Disc ◽  
Nucleus Pulposus ◽  
Cell Apoptosis ◽  
Redox Homeostasis ◽  
Mitochondrial Pathway ◽  
Nucleus Pulposus Cells ◽  
Damage Response ◽  
Induced Apoptosis ◽  
Ivd Degeneration

The death of nucleus pulposus (NP) cells is an important cause of intervertebral disc (IVD) degeneration. Redox disturbance caused by dysfunctional mitochondria has been considered as a vital risk for NP cell survival. It is valuable to identify key proteins maintaining mitochondrial function in NP cells. A previous study found that regulated in development and DNA damage response 1 (REDD1) are upregulated during intervertebral disc degeneration and that REDD1 can cause NP cell apoptosis. Thus, the present study further explores the effect of REDD1 on IVD degeneration. Our results showed that REDD1 promotes NP cell apoptosis via the mitochondrial pathway. Importantly, REDD1 formed a complex with TXNIP to strengthen its own action, and the combination was consolidated under H2O2-induced oxidative stress. The combined inhibition of the REDD1/TXNIP complex was better than that of REDD1 or TXNIP alone in restoring cell proliferation and accelerating apoptosis. Moreover, p53 acts as the transcription factor of REDD1 to regulate the REDD1/TXNIP complex under oxidative stress. Altogether, our results demonstrated that the REDD1/TXNIP complex mediated H2O2-induced human NP cell apoptosis and IVD degeneration through the mitochondrial pathway. Interferences on these sites to achieve mitochondrial redox homeostasis may be a novel therapeutic strategy for oxidative stress-associated IVD degeneration.

Effect of oxidative stress on fluoride-induced apoptosis in primary cultured Sertoli cells of rats

2014 ◽  
Vol 25 (1) ◽  
pp. 1-9 ◽  
Author(s):  
Yang Yang ◽  
Hui Huang ◽  
Yue Ba ◽  
Xue-Min Cheng ◽  
Liu-Xin Cui
Keyword(s):  
Oxidative Stress ◽  
Sertoli Cells ◽  
Induced Apoptosis

JNK and p38 MAPK regulate oxidative stress and the inflammatory response in chlorpyrifos-induced apoptosis

2013 ◽  
Vol 218 (3) ◽  
pp. 235-245 ◽  
Author(s):  
Yeo-Woon Ki ◽  
Jae Hyeon Park ◽  
Jeong Eun Lee ◽  
In Chul Shin ◽  
Hyun Chul Koh
Keyword(s):  
Oxidative Stress ◽  
Inflammatory Response ◽  
P38 Mapk ◽  
Induced Apoptosis

scholarly journals Diosgenin Induces Apoptosis in HepG2 Cells through Generation of Reactive Oxygen Species and Mitochondrial Pathway

2012 ◽  
Vol 2012 ◽  
pp. 1-8 ◽  
Author(s):  
Dae Sung Kim ◽  
Byoung Kook Jeon ◽  
Young Eun Lee ◽  
Won Hong Woo ◽  
Yeun Ja Mun
Keyword(s):  
P38 Mapk ◽  
Hepg2 Cells ◽  
Caspase 3 ◽  
Mitochondrial Pathway ◽  
Carcinoma Cells ◽  
Dapi Staining ◽  
Apoptotic Pathway ◽  
Induced Apoptosis ◽  
Dose Dependent ◽  
Human Hepatocellular Carcinoma Cells

Diosgenin, a naturally occurring steroid saponin found abundantly in legumes and yams, is a precursor of various synthetic steroidal drugs. Diosgenin is studied for the mechanism of its action in apoptotic pathway in human hepatocellular carcinoma cells. Based on DAPI staining, diosgenin-treated cells manifested nuclear shrinkage, condensation, and fragmentation. Treatment of HepG2 cells with 40 μM diosgenin resulted in activation of the caspase-3, -8, -9 and cleavage of poly-ADP-ribose polymerase (PARP) and the release of cytochromec.In the upstream, diosgenin increased the expression of Bax, decreased the expression of Bid and Bcl-2, and augmented the Bax/Bcl-2 ratio. Diosgenin-induced, dose-dependent induction of apoptosis was accompanied by sustained phosphorylation of JNK, p38 MAPK and apoptosis signal-regulating kinase (ASK)-1, as well as generation of the ROS. NAC administration, a scavenger of ROS, reversed diosgene-induced cell death. These results suggest that diosgenin-induced apoptosis in HepG2 cells through Bcl-2 protein family-mediated mitochndria/caspase-3-dependent pathway. Also, diosgenin strongly generated ROS and this oxidative stress might induce apoptosis through activation of ASK1, which are critical upstream signals for JNK/p38 MAPK activation in HepG2 cancer cells.

scholarly journals Role of oxidative stress in germ cell apoptosis induced by di(2-ethylhexyl)phthalate

2002 ◽  
Vol 365 (3) ◽  
pp. 849-856 ◽  
Author(s):  
Emiko KASAHARA ◽  
Eisuke F. SATO ◽  
Mami MIYOSHI ◽  
Ryusei KONAKA ◽  
Keiichi HIRAMOTO ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cytochrome C ◽  
Sertoli Cells ◽  
Phthalate Esters ◽  
Immunohistochemical Analysis ◽  
Synthetic Polymers ◽  
Oxygen Species ◽  
Induced Apoptosis ◽  
Ethylhexyl Phthalate

Phthalate esters have been used extensively as plasticizers of synthetic polymers. Recent studies have revealed that these esters induce atrophy of the testis, although its pathogenesis remains unknown. The present study describes the possible involvement of oxidative stress in the pathogenesis of atrophy of the rat testis induced by di(2-ethylhexyl)phthalate (DEHP). Biochemical and immunohistochemical analysis revealed that oral administration of DEHP increased the generation of reactive oxygen species, with concomitant decrease in the concentration of glutathione and ascorbic acid in the testis, and selectively induced apoptosis of spermatocytes, thereby causing atrophy of this organ. Oxidative stress was selectively induced in germ cells, but not in Sertoli cells, treated with mono(2-ethylhexyl)phthalate (MEHP), a hydrolysed metabolite of DEHP. Furthermore, MEHP selectively induced the release of cytochrome c from mitochondria of the testis. These results indicate that oxidative stress elicited by MEHP principally injured mitochondrial function and induced the release of cytochrome c, thereby inducing apoptosis of spermatocytes and causing atrophy of the testis.

Evidence of acrylamide- and glycidamide-induced oxidative stress and apoptosis in Leydig and Sertoli cells

2017 ◽  
Vol 36 (12) ◽  
pp. 1225-1235 ◽  
Author(s):  
BO Yilmaz ◽  
N Yildizbayrak ◽  
Y Aydin ◽  
M Erkan
Keyword(s):  
Oxidative Stress ◽  
Cell Viability ◽  
Sertoli Cells ◽  
Animal Health ◽  
Reproductive Toxicity ◽  
Significant Risk ◽  
Cell Types ◽  
Lactate Dehydrogenase Activity ◽  
Induced Apoptosis

Acrylamide (AA) is a common chemical, produced during food processing and widely used in various industries and laboratory processes. Thus, AA causes a significant risk for human and animal health. Recently published studies have suggested that reproductive toxicity of AA and glycidamide (GA) was mainly due to the oxidative stress which can lead to cell apoptosis. The present experiment was conducted to investigate the effect of oxidative stress on the apoptosis of mouse Leydig (TM3) and Sertoli (TM4) cells induced by AA and its metabolite GA. TM3 and TM4 cells were exposed to AA (10 µM and 1 mM) and GA (1 µM and 0.5 mM) for 24 h. Following the exposure time, the Leydig and Sertoli cells were evaluated for measurement of cell viability, lactate dehydrogenase activity, lipid peroxidation and hydrogen peroxide levels, apoptosis/necrosis rate, and mRNA expression levels of apoptotic genes (caspase3, Bcl-2, Bax, and p53). The present study showed that AA and GA exposure caused decrease in cell viability and increase in excessive oxidative stress and apoptosis in both cell types. In conclusion, our in vitro results demonstrate that oxidative stress probably plays a major role in AA- and GA-induced apoptosis of Leydig and Sertoli cells.

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