Effects of bisphenol A on the metabolisms of active oxygen species in mouse tissues

Kabuto, Hideaki; Hasuike, Satoru; Minagawa, Nobuko; Shishibori, Tsuyoshi

doi:10.1016/s0013-9351(03)00062-8

Cited by 210 publications

(177 citation statements)

References 15 publications

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“…In the present study, slight increase were observed in the MDA content after 24 h exposure to BPA; however, it was not statistically significant. Similar to our results, the increase in the MDA content in the tissues were not observed in mice, which were intraperitoneally injected with BPA (25 and 50 mg/kg/day for 5 days) despite a marked increase of ROS production [21]. On the other hand, in other studies, BPA has been reported to cause significant increases in lipid peroxidation in the liver of male rats orally exposed to BPA at doses of 0.2, 2.0, and 20 µg/kg/day for 30 days [5] and 25 mg/kg/ day for 50 days [25].…”

Section: Discussionsupporting

confidence: 91%

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Antioxidant defense system parameters in isolated fish hepatocytes exposed to bisphenol A — Effect of vitamin C

Kaya¹,

Kaptaner²

2016

Acta Biologica Hungarica

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In this study, isolated hepatocytes of pearl mullet (Alburnus tarichi) were exposed to bisphenol A (BPA) at concentrations of 25, 50, 100, and 200 µM for 24 h. Moreover, an in vitro antioxidant concentration of vitamin C (50 µM) was administrated to the culture medium along with the BPA exposures. Next, the antioxidant defense system parameters were analyzed. According to the results, the highest concentration of BPA (200 µM) proved to be severely toxic for the cells. The increased activities of superoxide dismutase (SOD) and glutathione-S-transferase (GST), the fluctuated activities of glutathione peroxidase (GPx), and the decreased content of reduced glutathione (GSH) were compared to the control group after the BPA exposures. Vitamin C co-administration was found to cause further increases in the SOD, GPx, and GST activities in some of the experimental groups and vitamin C could not restore the GSH content. Malondialdehyde (MDA) levels were observed to be unaffected in all exposure groups. These results show that BPA causes alterations in the antioxidant defenses of the isolated fish hepatocytes. In addition, vitamin C co-administration along with BPA was found to be non-protective against BPA-induced oxidative stress, consequently, aggravated a negative BPA impact.

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Section: Discussionsupporting

confidence: 91%

“…Similar to our findings, Hulak et al [17] reported increased SOD activities in the sterlet (Acipencer ruthenus) spermatozoa treated with BPA in vitro. The increases in the SOD activity could be due to superoxide anions [21]. GPx is the enzyme that reduces organic peroxides and hydroperoxides using GSH as a substrate [47].…”

Section: Discussionmentioning

confidence: 99%

Antioxidant defense system parameters in isolated fish hepatocytes exposed to bisphenol A — Effect of vitamin C

Kaya¹,

Kaptaner²

2016

Acta Biologica Hungarica

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“…Several findings indicate that BPA induces oxidative stress in many organs (Bindhumol et al, 2003;Kabuto et al, 2003). BPA facilitates the production of reactive oxygen species (ROS) and thus results in neuronal damage (Ooe et al, 2005;Lee et al, 2008).…”

Section: Mechanisms Of Bpamentioning

confidence: 99%

Effects of Prenatal and Neonatal Exposure to Bisphenol A on the Development of the Central Nervous System

Mizuo¹,

Narita²,

Miyagawa³

et al. 2010

Biomolecules and Therapeutics

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-Bisphenol A (BPA) is one of the most common endocrine disrupters. In the last decade, the number of studies concerning the effects of chronic treatment with BPA on the development of the central nervous system (CNS) has increased. However, little is known about the effects of chronic exposure to BPA on higher brain functions such as memory or psychomotor functions. Here, we report our following findings: (1) Prenatal and neonatal exposure to BPA enhances psychostimulant-induced rewarding effects, results in the up-or downregulation of dopamine receptors, causes memory impairment, and decreases choline acetyltransferase (ChAT) activity. (2) BPA activates astrocytes in vivo and in vitro. These findings suggest that prenatal and neonatal exposure to BPA affects the development of the CNS.

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“…These results were in harmony with Asahi et al, (2010) who assured that BPA increased the generation of reactive oxygen species. Also, Kabuto et al, (2003) found that BPA administration increases MDA levels in the tissue. Moreover, Morgan et al, (2014) revealed that BPA administration resulted in lipid peroxidation in kidney, brain and testicular tissues that was represented by the significantly increased MDA levels and reduced GSH concentrations.…”

Section: Discussionmentioning

confidence: 95%

“…Reactive oxygen species (ROS) are cytotoxic agents causing oxidative damage by attacking cell membrane and DNA (Kabuto et al, 2003). BPA can cause liver, kidneys, brain, and other organs injury by forming ROS, which are scavenged by the endogenous antioxidant defense system (Kabuto et al, 2004).…”

Section: Introductionmentioning

confidence: 99%

Impact of L-Carnitine on Bisphenol A-Induced Kidney Damage in Rats

Edres¹,

Taha²,

Mandour³

et al. 2018

AJVS

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Key words:Bisphenol A, L-carnitine, Malondialdehyde, Hydronephrosis, GlutathioneThe present study aimed to explore the protective effects of L-carnitine on the oxidative stress induced by Bisphenol A (BPA) in rat kidneys. Forty male adult rats were allocated into four groups (10 rats each); placebo, BPA (50 mg/kg bwt per os), Lcarnitine (500 mg/kg bwt i.p), and the BPA/L-carnitine-treated group. After 70 days, blood and kidneys were collected for measurement of renal function, oxidative/antioxidative status, histopathological analyses, and gene expression of nrf2. BPA significantly increased serum urea and carnitine levels suggesting renal damage evidenced by hydropic degenerative changes and hydronephrosis. The level of malondialdehyde (MDA) in kidney was elevated along with decline in renal total antioxidant capacity (TAC) and reduced glutathione (GSH) concentrations following challenged with BPA. Notably, the expression of nrf2 mRNA transcript in kidney tissues was down-regulated after BPA-induced toxicity. L-carnitine treatment ameliorates the damaged effects of BPA on kidneys as indicated by low levels of serum urea and carnitine, and renal MDA. Further, L-carnitine enhances the antioxidants (TAC, and GSH), with up-regulation of nrf2 expression in kidney tissues. Our results suggest the renoprotective activity of L-carnitine in BPA-induced kidney injuries through induction of antioxidant system and modulation of oxidative stress.

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Effects of bisphenol A on the metabolisms of active oxygen species in mouse tissues

Cited by 210 publications

References 15 publications

Antioxidant defense system parameters in isolated fish hepatocytes exposed to bisphenol A — Effect of vitamin C

Antioxidant defense system parameters in isolated fish hepatocytes exposed to bisphenol A — Effect of vitamin C

Effects of Prenatal and Neonatal Exposure to Bisphenol A on the Development of the Central Nervous System

Impact of L-Carnitine on Bisphenol A-Induced Kidney Damage in Rats

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