Bisphenol A exposure remodels cognition of male rats attributable to excitatory alterations in the hippocampus and visual cortex

Chen, Zhi; Li, Tingting; Zhang, Linke; Wang, Huan; Hu, Fan

doi:10.1016/j.tox.2018.10.002

Cited by 27 publications

(34 citation statements)

References 56 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Previous studies investigating ang ii and its receptors have primarily focused on the ang ii/aT1r axis (24)(25)(26)(27); therefore, the present study investigated the effects of BPa on hepatic damage and the ang ii/aT1r signaling pathway in a rat model of liver i/r injury. a previous study reported that 0.4 mg/kg/day BPa in rats is close to the current reference daily limit for human exposure by the u.S. environmental Protection agency (28). in another study assessing the effects of BPa on the cognitive function of rats, it was indicated that 0.4 mg/kg/day BPa caused a significant decline in spatial memory; however, anxiety-like behavior was only observed in the high-dose BPa group (4 mg/kg/day) (28).…”

Section: Discussionsupporting

confidence: 68%

“…a previous study reported that 0.4 mg/kg/day BPa in rats is close to the current reference daily limit for human exposure by the u.S. environmental Protection agency (28). in another study assessing the effects of BPa on the cognitive function of rats, it was indicated that 0.4 mg/kg/day BPa caused a significant decline in spatial memory; however, anxiety-like behavior was only observed in the high-dose BPa group (4 mg/kg/day) (28). a previous study investigating the effects of perinatal maternal exposure to BPa on the behavior of rat offspring, it was reported that male offspring in the 4 mg/kg group displayed significantly lower responses compared with control rats (29); therefore, 4 mg/kg BPa was used in the present study.…”

Section: Discussionsupporting

confidence: 68%

See 1 more Smart Citation

BPA disrupts 17‑estradiol‑mediated hepatic protection against ischemia/reperfusion injury in rat liver by upregulating the Ang�II/AT1R signaling pathway

Zhang

Shi

et al. 2020

Mol Med Report

View full text Add to dashboard Cite

Bisphenol a (BPa), a xenoestrogen commonly used in plastics, may act as an endocrine disruptor, which indicates that BPa might be a public health risk. The present study aimed to investigate the effect of BPa on 17β-estradiol (e2)-mediated protection against liver ischemia/reperfusion (i/r) injury, and to identify the underlying mechanisms using a rat model. a total of 56 male Sprague dawley rats were randomly divided into the following seven groups: i) Sham; ii) i/r; iii) Sham + BPa; iv) i/r + BPa; v) i/r + e2; vi) i/r + e2 + BPa; and vii) i/r + e2 + BPa + losartan [loS; an angiotensin ii (ang ii) type i receptor (aTir) antagonist]. a rat model of hepatic i/r injury was established by inducing hepatic ischemia for 60 min followed by reperfusion for 24 h. When ischemia was induced, rats were treated with vehicle, e2, BPa or loS. after 24 h of reperfusion, blood samples and hepatic tissues were collected for histopathological and biochemical examinations. The results suggested that 4 mg/kg BPA did not significantly alter the liver function, or Ang II and aT1r expression levels in the Sham and i/r groups. However, 4 mg/kg BPa inhibited e2-mediated hepatic protection by enhancing hepatic necrosis, and increasing the release of alanine transaminase, alkaline phosphatase and total bilirubin (P<0.05). Moreover, BPa increased serum and hepatic ang ii levels, as well as aT1r protein expression levels in the e2-treated rat model of liver i/r injury (P<0.05). loS treatment reversed the negative effects of BPa on hepatic necrosis and liver serum marker levels, although it did not reverse BPa-mediated upregulation of serum and hepatic ang ii levels, or hepatic aT1r expression. Therefore, the present study suggested that BPa disrupted e2-mediated hepatic protection following i/R injury, but did not significantly affect healthy or i/r-injured livers; therefore, the mechanism underlying the effects of BPa may be associated with upregulation of the ang ii/aT1r signaling pathway.

show abstract

Section: Discussionsupporting

confidence: 68%

Section: Discussionsupporting

confidence: 68%

BPA disrupts 17‑estradiol‑mediated hepatic protection against ischemia/reperfusion injury in rat liver by upregulating the Ang�II/AT1R signaling pathway

Zhang

Shi

et al. 2020

Mol Med Report

View full text Add to dashboard Cite

show abstract

“…9 The reported underlying mechanisms comprised oxidative stress and lipid peroxidative capacity, decreased acetylcholinesterase activity, increased apoptosis, decreased glutamate receptors expression, and suppressed cAMP response element-binding protein (CREB) and brain-derived neurotrophic factor (BDNF) phosphorylation. [10][11][12][13] Experimental studies have shown protective effects of natural antioxidants such as curcumin and lipoic acid against BPA-induced cognitive and other neurobehavioral disturbances. 13,14 Lycopene, on the other hand, is an aliphatic hydrocarbon carotenoid that can be found in different fruits and vegetables, for example, watermelon and tomatoes.…”

Section: Introductionmentioning

confidence: 99%

Protective effects of lycopene on hippocampal neurotoxicity and memory impairment induced by bisphenol A in rats

Morsy

Ahmed

2020

Hum Exp Toxicol

View full text Add to dashboard Cite

Bisphenol A (BPA) is used to produce polycarbonate plastic and epoxy resins which are used in many consumer products. Most people encounter BPA in their daily routines. However, it has been heavily reported that BPA has a neurotoxic effect. The present study aimed to investigate the effect of lycopene on cognitive deficits induced by a high dose of BPA focusing on mitogen-activated protein kinase (MAPK)/extracellular signal-regulated kinase (ERK) pathway, oxidative stress, apoptosis, and memory retrieval in adult male rats. Therefore, 72 rats were divided into four groups: control group, BPA group (50 mg/kg body weight (bw)) 3 days a week for 42 days, lycopene group (10 mg/kg bw) daily for 42 days, and lycopene + BPA group. Concurrent treatment of lycopene with BPA improved the learning and cognition memory in Morris water maze and novel object recognition tests along with an increase in acetylcholine esterase activity as well as inhibition of oxidative stress by restoring reduced glutathione and suppressing malondialdehyde hippocampal level to their normal levels. Mechanistically, lycopene upregulated the protein expression of tyrosine receptor kinase B, which resulted in an upsurge in its downstream cascades MAPK/ERK1/2/cAMP response element-binding protein (CREB)/brain-derived neurotrophic factor (BDNF) signaling pathway in the hippocampus of BPA-intoxicated rats. Furthermore, concurrent treatment of lycopene with BPA prevented apoptosis by marked decrease in Bcl-2 associated X protein (Bax) gene expression and caspase 3 activity while restoring B-cell leukemia/lymphoma-2 (Bcl-2) gene expression. In conclusion, the present study provided evidence that lycopene exerted a neuroprotective effect against BPA intoxication in hippocampi of rats via its antioxidant properties, activation of MAPK/ERK pathway, and inhibiting a neuronal apoptosis which reflected on improving the learning and cognition memory.

show abstract

“…Chen et al found that juvenile BPA exposure impairs the spatial memory only in male rats, in a dose and gender-dependent manner. Such cognitive impairment was due to changes of the excitatory plasticity, such as the downregulated spine density and glutamate receptor expression levels in the hippocampus [88]. High concentrations of BPA (>100 µM) exposure in mice hippocampal HT-22 cells induces apoptosis by increasing the calcium influx and ROS levels, followed by activating the phosphorylation of extracellular signal-regulated kinase, c-Jun N-terminal kinase, and caspase 3 [133].…”

Section: Neurotoxicitymentioning

confidence: 99%

Bisphenols as a Legacy Pollutant, and Their Effects on Organ Vulnerability

Kim

Kumar

et al. 2019

IJERPH

View full text Add to dashboard Cite

Bisphenols are widely used in the synthesis of polycarbonate plastics, epoxy resins, and thermal paper, which are used in manufacturing items of daily use. Packaged foods and drinks are the main sources of exposure to bisphenols. These chemicals affect humans and animals by disrupting the estrogen, androgen, progesterone, thyroid, and aryl hydrocarbon receptor functions. Bisphenols exert numerous harmful effects because of their interaction with receptors, reactive oxygen species (ROS) formation, lipid peroxidation, mitochondrial dysfunction, and cell signal alterations. Both cohort and case-control studies have determined an association between bisphenol exposure and increased risk of cardiovascular diseases, neurological disorders, reproductive abnormalities, obesity, and diabetes. Prenatal exposure to bisphenols results in developmental disorders in animals. These chemicals also affect the immune cells and play a significant role in initiating the inflammatory response. Exposure to bisphenols exhibit age, gender, and dose-dependent effects. Even at low concentrations, bisphenols exert toxicity, and hence deserve a critical assessment of their uses. Since bisphenols have a global influence on human health, the need to discover the underlying pathways involved in all disease conditions is essential. Furthermore, it is important to promote the use of alternatives for bisphenols, thereby restricting their uses.

show abstract

Bisphenol A exposure remodels cognition of male rats attributable to excitatory alterations in the hippocampus and visual cortex

Cited by 27 publications

References 56 publications

BPA disrupts 17‑estradiol‑mediated hepatic protection against ischemia/reperfusion injury in rat liver by upregulating the Ang�II/AT1R signaling pathway

BPA disrupts 17‑estradiol‑mediated hepatic protection against ischemia/reperfusion injury in rat liver by upregulating the Ang�II/AT1R signaling pathway

Protective effects of lycopene on hippocampal neurotoxicity and memory impairment induced by bisphenol A in rats

Bisphenols as a Legacy Pollutant, and Their Effects on Organ Vulnerability

Contact Info

Product

Resources

About