Nuclear factor erythroid 2-related factor 2 rescues the oxidative stress induced by di-<i>N</i>-butylphthalate in testicular Leydig cells

Shen, Baixin; Wang, W; Ding, Ling; Sao, Yunpeng; Huang, Yi; Zheng, Shen; Zhuo, Yisha; Wei, Zuoan; Zhang, W

doi:10.1177/0960327114530744

Cited by 21 publications

(10 citation statements)

References 18 publications

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“…SFN is a strong stimulant for Nrf2 and could exert potent antioxidant activity by activating Nrf2 . We first found that SFN induced similar extent of Nrf2 level to lentiviral Nrf2 overexpression and was paralleled with down‐regulation of KEAP1 (Fig.…”

Section: Resultsmentioning

confidence: 85%

Nrf2 sensitizes prostate cancer cells to radiation via decreasing basal ROS levels

Liu

Yao

et al. 2015

BioFactors

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Androgen deprivation therapy (ADT) was reported to lower basal ROS level in prostate cancer (PCa) and to sensitize PCa to radiation. We aimed to seek for the underlying molecular mechanism and to develop novel additive treatments to ADT in this regard. We simulated human androgen milieu in vitro and tested the ROS level in PCa cells undergoing ADT. We also tested the Nrf2 level in PCa cells with or without ADT. Genetic and pharmaceutical upregulation of Nrf2 was applied in vitro and in vivo in transgenic adenocarcinoma of the mouse prostate (TRAMP) mice with or without castration to investigate whether Nrf2 overexpression supplemented the effect of ADT in PCa. We first discovered that androgen deprivation increased basal ROS level in PCa cells with AR expression. We then found that genetic Nrf2 upregulation lowered basal ROS similar to ADT. Also, SFN sensitized PCa cell to radiation via upregulation of Nrf2. We then found that Nrf2 level in control TRAMP groups was lower than castration or SFN groups. The SFN treated TRAMP mice showed similar level of Nrf2 to castration. Genetic and pharmaceutical upregulation of Nrf2 lowered the ROS in PCa cells and sensitized PCa cells to radiation similar to ADT, implicating possible administration of SFN in place of ADT for PCa patients requiring radiotherapy.

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Section: Resultsmentioning

confidence: 85%

Nrf2 sensitizes prostate cancer cells to radiation via decreasing basal ROS levels

Liu

Yao

et al. 2015

BioFactors

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“…Thus, we suggest that DBP may cause testis injuries via oxidative stress. Importantly, we have previously carried out a series of experiments by stimulation of DBP on a cell model, and have found that DBP could cause testicular oxidative stress injury and antioxidant drugs might resist this damage [ 7 ]. Therefore, we used the pregnant mice as a research model to study the impact of exposure to DBP and explore the protective effects of SFN.…”

Section: Discussionmentioning

confidence: 99%

“…Amid all organs, DBP has the highest affinity for testes and induces the oxidative stress injury, causing male reproductive dysfunction [ 5 , 6 ]. Our previous studies have suggested DBP could induce oxidative stress injury in testicular Leydig cells [ 7 ].…”

Section: Introductionmentioning

confidence: 99%

Protective effects of sulforaphane on di-n-butylphthalate-induced testicular oxidative stress injury in male mice offsprings via activating Nrf2/ARE pathway

et al. 2017

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Di-N-butylphthalate (DBP) is one of the most common endocrine-disrupting chemicals which can disrupt human endocrine system, especially in the male reproductive system. Here, this study was aimed to determine whether sulforaphane (SFN) could protect against testicular oxidative stress injury induced by DBP in male mice offsprings. Wild-type (Nrf2+/+) and Nrf2-deficient (Nrf2-/-) timed-pregnant mice were given DBP orally from embryonic day (E)14.5 to E19.5. Subsequently, the oxidative stress markers were evaluated. Besides, Nrf2, NF-κB, I-kB, HO-1 and NQO-1 expression levels in the testis were measured by immunohistochemical staining or western blot analysis. DBP significantly reduced anogenital distance (AGD) and influenced testes growth in male mice offsprings, while SFN ameliorated these phenotypes. After DBP stimulation, the testicular morphology, testicular cell apoptosis index and the oxidative stress markers exhibited statistical differences compared with Control group, while SFN supplementation showed obvious improvements. In addition, administration of SFN could obviously increase the expression level of Nrf2 and its downstream ARE gene battery, such as HO-1, NQO-1 in the testis. Meanwhile, SFN pretreatment did not confer protection against DBP-induced testicular oxidative stress injury in Nrf2 knockout mice. Therefore, the present findings suggested that SFN could effectively protect against DBP-induced testicular oxidative stress injury through Nrf2/ARE signaling pathways in male mice offsprings.

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“…The 'tube restraint test' was carried out and a significant change in the latency to the first bite and in the number of targets biting by the Pb treated female offspring. Recently other report suggested that the aggressive behaviour of mice was increased after exposing to lead acetate in their drinking water [18]. Anxiety is generally described as a physiological, behavioural and psychological state induced in humans and animals by a threat to well-being, potential or either actual.…”

Section: Social and Anxiety Behaviourmentioning

confidence: 99%

CURCUMIN ATTENUATES LEAD (Pb)–INDUCED NEUROBEHAVIORL AND NEUROBIOCHEMICAL DYSFUNCTION: A REVIEW

Abu-Taweel

2018

Int J Pharm Pharm Sci

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Lead is one of the common chemical elements that is assigned the symbol Pb which came from the Latin Plumbum. Pb is widely used in the field of coating, refine and glaze ceramics and pottery. It is still used in the production of products like water pipes, cooking utensils and cooking utensils. In addition it is also used in insulation of building ceilings, cable coverage and military industries. Lead enter the environment from those uses and from the environment it enter into the living organisms. Lead accumulates in many humanorgans, but the brain is the target organ of lead accumulation. Neurotoxicity of lead is, one of lead toxicity, caused many symptoms. There are many behavioral and biochemical modifications induced by lead toxicity like learning and memory deficits, anxiety disorders, social and sexual behavior modifications and neurotransmitter system deficits. Curcumin is a bioactive natural phytochemical phenolic compound (diferuloylmethane) extracted from the rhizome of Curcuma longa. Most studies indicated the role of curcumin in reducing the damage of lead toxicity. In the current review, emphasis was based on the toxicity of lead and its effect on behavior and some neurotransmitters related to behavior. The effect of curcumin is improving the neurotoxicity and behavioral toxicity of lead.

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Nuclear factor erythroid 2-related factor 2 rescues the oxidative stress induced by di-N-butylphthalate in testicular Leydig cells

Cited by 21 publications

References 18 publications

Nrf2 sensitizes prostate cancer cells to radiation via decreasing basal ROS levels

Nrf2 sensitizes prostate cancer cells to radiation via decreasing basal ROS levels

Protective effects of sulforaphane on di-n-butylphthalate-induced testicular oxidative stress injury in male mice offsprings via activating Nrf2/ARE pathway

CURCUMIN ATTENUATES LEAD (Pb)–INDUCED NEUROBEHAVIORL AND NEUROBIOCHEMICAL DYSFUNCTION: A REVIEW

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