Lutein alleviates arsenic-induced reproductive toxicity in male mice via Nrf2 signaling

Li, S G; Xu, Shangzhi; Niu, Qiang; Ding, Yaobin; Pang, Lijuan; L, R; Jing, Mingxia; Wang, K; M, X; Feng, Gangling; Liu, J M; Zhang, X F; Xiang, Hui; Li, F

doi:10.1177/0960327115595682

Cited by 43 publications

(28 citation statements)

References 39 publications

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“… 19 Similarly, disproportionate induction of NQO1 and Nrf2 by As 2 O 3 has been reported in male Kunming mouse testis in both the presence and absence of antioxidants such as lutein. 20 …”

Section: Resultsmentioning

confidence: 99%

Modulation of Cellular Response to Arsenic Trioxide Toxicity by Resveratrol

et al. 2018

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Arsenic trioxide (As2O3) is an environmental carcinogen and a putative endocrine disruptor. Resveratrol has been shown to reverse As2O3-induced oxidative damage. In immortalized but nontransformed estrogen receptor α-negative human breast cells (MCF10A), we observed that 25 μM resveratrol ameliorated As2O3-induced cytotoxicity. As2O3, in the presence or absence of 25 μM resveratrol, induced quinone reductase (NAD(P)H quinone dehydrogenase 1), via the induction of NFE2-related factor 2. As2O3 caused a repression of cytochrome P450 (CYP)1B1, but the addition of 25 μM resveratrol rescued the expression of cytochrome P450 1B1 and kept it at a constant level. Therefore, 25 μM resveratrol can modulate the effects of As2O3 on enzymes involved in estrogen metabolism.

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“… 19 Similarly, disproportionate induction of NQO1 and Nrf2 by As 2 O 3 has been reported in male Kunming mouse testis in both the presence and absence of antioxidants such as lutein. 20 …”

Section: Resultsmentioning

confidence: 99%

Modulation of Cellular Response to Arsenic Trioxide Toxicity by Resveratrol

et al. 2018

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“…Attenuation of neuroinflammation in micro-glia cells by lutein was mediated through inhibition of NF-κB activation and activation of Nrf2 levels [ 30 ]. Lutein prevented arsenic-induced reproductive toxicity through enhancing Nrf2 levels and their target proteins HO-1, NQO1 and GST [ 31 ].…”

Section: Discussionmentioning

confidence: 99%

Lutein prevents osteoarthritis through Nrf2 activation and downregulation of inflammation

Qiao¹,

Jiang²,

Gao³

2018

aoms

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IntroductionOsteoarthritis is an inflammatory disorder associated with oxidative stress and apoptosis leading to cartilage destruction and impairment of cartilage formation. In the present study, we studied the protective effect of lutein against monosodium iodoacetate (MIA)-induced osteoarthritis in primary chondrocyte cells.Material and methodsOxidative stress was determined through testing antioxidant status, reactive oxygen species levels and lipid peroxide content. Also, Nrf2 expression and its downstream target genes HO-1 and NQO-1 were determined. Inflammation was analyzed through NF-κB, COX-2 and pro-inflammatory cytokines (IL-6, TNF-α, IL-1β). In addition, the effects of MIA and lutein on mitochondrial membrane potential and caspase-3 levels were analyzed.ResultsThe results showed that lutein treatment significantly increased the cell viability of chondrocytes and offered significant cytoprotection by enhancing the antioxidant defense mechanisms and reducing oxidative stress (reactive oxygen species and lipid peroxidation). Lutein treatment showed anti-inflammatory effects by downregulating inflammatory proteins (NF-κB, COX-2) and pro-inflammatory cytokines (IL-6, TNF-α, IL-1β). Lutein reduced MIA-induced apoptosis through maintaining mitochondrial membrane potential and downregulating caspase-3 activity.ConclusionsThe present study shows significant cytoprotection offered by lutein against MIA-induced oxidative stress, inflammation and apoptosis by the modulatory effect of NF-κB and Nrf2 activation.

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“…Recently, Li et al (2016) showed that 5 mg/kg/day As 2 O 3 treatment of mice for 35 days reduced normal sperm number. In agreement with these findings Xia, Hao, and Yang (2009) noted that these effects also occurred in rats treated with 4 or 8 mg/ kg/day as the rate of malformed sperm was elevated.…”

Section: Discussionmentioning

confidence: 99%

Arsenic trioxide exposure impairs testicular morphology in adult male mice and consequent fetus viability

Silva

Borges

Lamas

et al. 2017

Journal of Toxicology and Environmental Health, Part A

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The acute promyelocytic leukemia (APL) is a rare disease, affecting 0.1/100,000 individuals globally. Despite significant advances in APL therapy, some patients still experience relapsed disease. Currently, arsenic trioxide (AsO) was found to be effective in relapsed APL treatment and considered as standard treatment for these cases. However, it has been shown that exposure to AsO may exert adverse effects on the male reproductive system since this substance might also induce apoptosis of other important cell types including stem cells. Studies demonstrated that treatment with this metallic substance decreased plasma levels of testosterone and interfered with sperm parameters such as concentration, motility, and viability. In addition, AsO was found to produce significant damage to spermatocytes, which may be associated with testicular toxicity and consequent inhibition of spermatogenesis. The aim of this study was to determine sub-chronic treatment effects of AsO on sperm and testicular morphology, androgen receptor (AR) immunoreactivity in testes and epididymis, in addition to evaluation of fertility parameters in adult male mice. Thirty adult Swiss mice were divided into three experimental groups: control; received distilled water (vehicle) while treated received 0.3 or 3 mg/kg/day AsO subcutaneously, for 5 days per week, followed by 2 days of interruption, for 5 weeks. Results showed that AsO (1) decreased spermatozoa number, (2) produced seminiferous epithelium degeneration and exfoliation of germ cells tubule lumen (3) altered nucleus/cytoplasm proportion of Leydig cells and (4) reduced AR immunoreactivity in both Leydig and epithelial epididymal cells. Further, fetal viability tests demonstrated an increase in post-implantation loss in females that were mated with AsO-treated males. Data indicate that AsO exposure altered the spermatogenic process and subsequently fetal viability.

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Lutein alleviates arsenic-induced reproductive toxicity in male mice via Nrf2 signaling

Cited by 43 publications

References 39 publications

Modulation of Cellular Response to Arsenic Trioxide Toxicity by Resveratrol

Modulation of Cellular Response to Arsenic Trioxide Toxicity by Resveratrol

Lutein prevents osteoarthritis through Nrf2 activation and downregulation of inflammation

Arsenic trioxide exposure impairs testicular morphology in adult male mice and consequent fetus viability

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