Perfluorooctanoic acid exposure alters polyunsaturated fatty acid composition, induces oxidative stress and activates the AKT/AMPK pathway in mouse epididymis

Lu, Yin; Pan, Yitao; Sheng, Nan; Zhao, Allan Z.; Dai, Jiayin

doi:10.1016/j.chemosphere.2016.05.071

Cited by 38 publications

(22 citation statements)

References 73 publications

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“…Several studies have demonstrated that PFOA is able to generate oxidative stress in various cell types and organisms . In our study, it was found that ROS levels increased significantly and in a concentration‐dependent manner in PFOA‐exposed ovaries ex vivo.…”

Section: Discussionsupporting

confidence: 62%

“…Animal studies have also shown that exposure to PFOA generates oxidative stress and apoptosis in vitro and in vivo: PFOA exposure significantly inhibited luteal function via oxidative stress and apoptosis in pregnant mice, induced oxidative stress in mouse epididymis and ROS elevation in isolated rat liver and brain mitochondria . The role of ROS within the female reproductive system is complex.…”

Section: Introductionmentioning

confidence: 99%

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Perfluorooctanoic acid disrupts gap junction intercellular communication and induces reactive oxygen species formation and apoptosis in mouse ovaries

López-Arellano

Luna

et al. 2018

Environmental Toxicology

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Perfluorooctanoic acid (PFOA) is a member of the perfluoroalkyl acid family of compounds. Due to the presence of strong carbon-fluorine bonds, it is practically nonbiodegradable and highly persistent in the environment. PFOA has been detected in the follicular fluid of women, and positively associated with reduced fecundability and infertility. However, there are no reports concerning the experimental evaluation of PFOA on oocyte toxicity in mammals. The aim of the present study was to determine if PFOA is able to induce oxidative stress in fetal ovaries and cause apoptosis in oocytes in vitro. In addition, since inhibition of the gap junction intercellular communication (GJIC) by PFOA has been demonstrated in liver cells in vivo and in vitro, the effect of PFOA on the GJIC between the oocyte and its supportive cumulus cells was studied.Results show that PFOA induced oocyte apoptosis and necrosis in vitro (medium lethal concentration, LC 50 = 112.8 μM), as evaluated with Annexin-V-Alexa 508 in combination with BOBO-1 staining. Reactive oxygen species (ROS) levels, as assessed by DCFH-DA, increased significantly in fetal ovaries exposed to ¼ LC 50 (28.2 μM, a noncytotoxic and relevant occupational exposure concentration) and LC 50 PFOA ex vivo. This perfluorinated compound also caused the blockage of GJIC in cumulus cells-oocyte complexes (COCs) obtained from female mice exposed in vivo, as evaluated by calcein transfer from cumulus cells to the oocyte. The ability of PFOA of disrupting the GJIC in COCs, generating ROS in the fetal ovary and causing apoptosis and necrosis in mammal's oocytes, might account for the reported association between increasing maternal plasma concentrations of PFOA with reduced fertility in women.

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Section: Discussionsupporting

confidence: 62%

Section: Introductionmentioning

confidence: 99%

Perfluorooctanoic acid disrupts gap junction intercellular communication and induces reactive oxygen species formation and apoptosis in mouse ovaries

López-Arellano

Luna

et al. 2018

Environmental Toxicology

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“…Perfluoropentanoic acid (PFPA), PFOA, and perfluorodecanoic acid (PFDA)‐induced oxidative stress via reducing GSH content and the activities of SOD and CAT in human erythrocytes . PFOA treatment resulted in oxidative stress in the epididymis and increased ROS levels in sperm in vitro . in vivo exposure of PFOS significantly increased intracellular ROS production, but weakened intracellular antioxidant defense by inhibiting catalase and superoxide dismutase activities in the liver .…”

Section: Discussionmentioning

confidence: 99%

8:2 Fluorotelomer alcohol causes immunotoxicity and liver injury in adult male C57BL/6 mice

Wang

Kong

et al. 2018

Environmental Toxicology

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8:2 Fluorotelomer alcohol (8:2 FTOH) is widely used in houseware and industrial goods and is ubiquitous in the surrounding environment. 8:2 FTOH has been linked to hepatoxicity, nephrotoxicity, and reproductive toxicity, as well as endocrine-disrupting effects. However, as of yet, the research regarding immunotoxicity of 8:2 FTOH remains largely limited. In the present study, adult male C57BL/6 mice were administered with 10, 30, and 100 mg/kg/d 8:2 FTOH by gavage for 28 days to investigate its immunotoxicity in vivo. The results showed that exposure to 8:2 FTOH caused increases in liver weight and histological changes in the liver, including vacuolation, cell swelling, immune cell infiltration, karyopyknosis and nuclear swelling. No histological change in either the spleen or the thymus was observed after administration of 8:2 FTOH. In addition, exposure to 8:2 FTOH reduced the concentration of IL-1β in serum, and mRNA levels of IL-1β, IL-6, and TNF-α in both the thymus and spleen. CXCL-1 mRNA expression was downregulated in both the liver and thymus after 8:2 FTOH administration, while only IL-1β mRNA expression was upregulated in the liver. Moreover, the exposure of primary cultured splenocytes to 8:2 FTOH inhibited the ConA-stimulated proliferation of splenocytes at concentrations of 30 and 100 μM, and the LPS-stimulated proliferation of splenocytes at 100 μM. Furthermore, 8:2 FTOH inhibited the level of secreted IFN-γ in ConA-stimulated splenocytes. The results obtained in the study demonstrated that 8:2 FTOH posed potential immunotoxicity and liver injury in mice. Our findings will provide novel data for the health risk assessment of 8:2 FTOH. K E Y W O R D S 8:2 FTOH, immunotoxicity, liver injury, mice, oxidative stress 1 | INTRODUCTION Fluorotelomers, as fluorocarbon-based oligomers or telomers, have various applications in food packaging, home furnishings, fire-fighting foams, surfactants, textiles, adhesives, waxes, polishes, and leather. 1 It was reported that the market size of fluorotelomers was 26.5 kt in 2015, and its annual growth rate is estimated to be 12.7%. 2 Among fluorotelomers, fluorotelomer alcohol (FTOH) products dominate global consumption; these products reportedly made up approximately 32% of the overall volume of fluorotemomers in 2013. 3 8:2 FTOH is the most abundant FTOH homologue and is ubiquitous in the environment. 4 Chen et al. 5 detected FTOHs in several wastewater treatment plants in China, and the study also found that 8:2 FTOH was the primary FTOH in the influent, secondary effluent, and sludge, with the concentrations ranging from 2.10 to 11.0 ng/L, 3.05 to 12.4 ng/L, and 0.36 to 1.91 ng/g dry weight, respectively. Bach et al. 6 assessed 14 perfluorinated compounds (PFCs) in water samples in France and found that the concentrations of 8:2 FTOH were 117 ng/L and 213 ng/L in tap and surface water, respectively. Additionally, 8:2 FTOH was commonly detected in food contact materials (FCMs). For example, 8:2 FTOH was detected in most Chinese and American FCM samples at concentra...

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“…As a stable compound extensively distributed in the environment, PFOA has been suggested to induce male reproductive dysfunction in humans and animals. [11][12][13][14][15][16] Que, a natural antioxidant, has received considerable attention due to its potential health benets. The presence of the catechol moiety and free hydroxyl groups in the Que structure is responsible for its antioxidant and free radical scavenger potential.…”

Section: Discussionmentioning

confidence: 99%

“…11 Furthermore, a study of 105 young men indicated that high levels of serum PFOA-PFOS were associated with reduced numbers of normal spermatozoa. 12 In animal experiments, PFOA has been shown to disrupt blood-testis barrier, 13 destroy testicular steroidogenic machinery, 14 and alter polyunsaturated fatty acid composition and induce oxidative stress in mouse epididymis, 15 thus resulting in male reproductive dysfunction. We also reported previously that exposure to PFOA disrupted spermatogenesis through inducing testicular oxidative stress and apoptosis in mice.…”

Section: Introductionmentioning

confidence: 99%

Attenuation of perfluorooctanoic acid-induced testicular oxidative stress and apoptosis by quercetin in mice

Yuan

et al. 2017

RSC Adv.

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Perfluorooctanoic acid exposure alters polyunsaturated fatty acid composition, induces oxidative stress and activates the AKT/AMPK pathway in mouse epididymis

Cited by 38 publications

References 73 publications

Perfluorooctanoic acid disrupts gap junction intercellular communication and induces reactive oxygen species formation and apoptosis in mouse ovaries

Perfluorooctanoic acid disrupts gap junction intercellular communication and induces reactive oxygen species formation and apoptosis in mouse ovaries

8:2 Fluorotelomer alcohol causes immunotoxicity and liver injury in adult male C57BL/6 mice

Attenuation of perfluorooctanoic acid-induced testicular oxidative stress and apoptosis by quercetin in mice

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