Alterations in the memory of rat offspring exposed to low levels of fluoride during gestation and lactation: Involvement of the α7 nicotinic receptor and oxidative stress

Bartos, Mariana; Gumilar, Fernanda; Gallegos, Cristina Eugenia; Bras, Cristina; Domínguez, Sergio; Mónaco, Nina; Esandi, María del Carmen; Bouzat, Cecilia; Cancela, Liliana Marina; Minetti, Alejandra

doi:10.1016/j.reprotox.2018.07.078

Cited by 24 publications

(24 citation statements)

References 63 publications

(97 reference statements)

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“…cAMP response element-binding protein (CREB), and Brain-derived Neurotrophic factor (BDNF) levels in the hippocampus (32). CUR has been shown to significantly improve spatial memory impairment induced by human immunodeficiency viruses-1 (HIV-1) in rats, but the electrophysiological mechanism remains unknown (33).…”

Section: Discussionmentioning

confidence: 99%

Effect of curcumin on hippocampus dentate gyrus injury induced by nicotine in rats

Jalili

Rodsari

Roshankhah

et al. 2019

J Herbmed Pharmacol

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Introduction: Nicotine is the most important alkaloid compound in tobacco and is a major risk factor in the development of functional disorder of several organ systems. Some plants produce Curcumin, which has antioxidant and neuroprotective properties. This study was designed to evaluate the therapeutic effects of curcumin against nicotine injury on the hippocampus CA1 region of rats. Methods: In this study, 48 male Wistar rats were randomly assigned to eight groups: Normal control (saline) group, Nicotine control group (0.5 mg/kg); Curcumin groups (10, 30, and 60 mg/kg) and Nicotine + Curcumin groups (10, 30, and 60 mg/kg). Treatments were administered intraperitoneally daily for 28 days. Golgi staining technique investigated the number of dendritic spines. Cresyl violet staining method was used to determine the number of neurons in hippocampal region CA1. Griess technique was assessed to determine serum nitrite oxide level. Also, the Ferric reducing/antioxidant power (FRAP) method was applied to determine the total antioxidant capacity. Results: Nicotine administration significantly increased nitrite oxide level and decreased total antioxidant capacity as well as the number of neuronal dendritic spines and neurons compared to the normal control group (P < 0.01). In all Curcumin and Nicotine + Curcumin groups, the number of neurons, neuronal dendritic spines, and total antioxidant capacity increased significantly compared to the nicotine control group, while nitrite oxide level decreased significantly compared to the nicotine control group (P < 0.01). Conclusion: Curcumin administration can improve hippocampal CA1 region injury induced by nicotine.

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Section: Discussionmentioning

confidence: 99%

Effect of curcumin on hippocampus dentate gyrus injury induced by nicotine in rats

Jalili

Rodsari

Roshankhah

et al. 2019

J Herbmed Pharmacol

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“…Eight studies published since 2017 investigated the effect of fluoride on learning and memory following exposure during development (Bartos et al 2018;Chen et al 2018a;Ge et al 2018;McPherson et al 2018;Mesram et al 2017;Sun et al 2018;Wang et al 2018;Zhao et al 2019); and five additional studies examined exposure during young Sprando et al (1997Sprando et al ( , 1998 adulthood (Dong et al 2017;Li et al 2019;Pulungan et al 2018;Sharma et al 2018a;Yang et al 2018). Only one study among them was conducted according to the generally accepted guidelines considering all of the aforementioned key requirements (McPherson et al 2018).…”

Section: Neurobehavioral Studies and Neurotoxicitymentioning

confidence: 99%

“…Some reports suggest that NaF has an effect on learning and memory. Six studies in rats (Bartos et al 2018;Chen et al 2018a;Dong et al 2017;Mesram et al 2017;Yang et al 2018;Zhao et al 2019) and five in mice (Ge et al 2018;Li et al 2019;Sharma et al 2018a;Sun et al 2018;Wang et al 2018) reported such effects (mainly by investigating maze performance, e.g., MWM) with 20-120 mg/L NaF (9-54 mg/L fluoride) in drinking water corresponding to doses of approximately 0.46-6.1 mg/kg b.w./day. However, these studies had several limitations: two did not give adequate information with regard to the four key requirements (Ge et al 2018;Wang et al 2018).…”

Section: Neurobehavioral Studies and Neurotoxicitymentioning

confidence: 99%

“…The overall reporting of data was insufficient and indicative of a high risk of bias. The remaining studies also revealed one to three of the key limitations (Table 4), e.g., lack of reporting of blinding (Bartos et al 2018;Li et al 2019;Mesram et al 2017;Sharma et al 2018a;Sun et al 2018) or randomization (Sharma et al 2018a), lack of controlling for litter effects (Chen et al 2018a;Mesram et al 2017;Sun et al 2018;Zhao et al 2019), or the lack of a clear characterization of the test compound, i.e., whether concentrations or dose levels refer to fluoride or sodium fluoride (Bartos et al 2018;Dong et al 2017;Mesram et al 2017;Yang et al 2018). Furthermore, only a single dose was investigated in several studies (Dong et al 2017;Li et al 2019;Mesram et al 2017;Sharma et al 2018a), which was identified as the LOAEL.…”

Section: Neurobehavioral Studies and Neurotoxicitymentioning

confidence: 99%

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Toxicity of fluoride: critical evaluation of evidence for human developmental neurotoxicity in epidemiological studies, animal experiments and in vitro analyses

et al. 2020

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Recently, epidemiological studies have suggested that fluoride is a human developmental neurotoxicant that reduces measures of intelligence in children, placing it into the same category as toxic metals (lead, methylmercury, arsenic) and polychlorinated biphenyls. If true, this assessment would be highly relevant considering the widespread fluoridation of drinking water and the worldwide use of fluoride in oral hygiene products such as toothpaste. To gain a deeper understanding of these assertions, we reviewed the levels of human exposure, as well as results from animal experiments, particularly focusing on developmental toxicity, and the molecular mechanisms by which fluoride can cause adverse effects. Moreover, in vitro studies investigating fluoride in neuronal cells and precursor/stem cells were analyzed, and 23 epidemiological studies published since 2012 were considered. The results show that the margin of exposure (MoE) between no observed adverse effect levels (NOAELs) in animal studies and the current adequate intake (AI) of fluoride (50 µg/kg b.w./day) in humans ranges between 50 and 210, depending on the specific animal experiment used as reference. Even for unusually high fluoride exposure levels, an MoE of at least ten was obtained. Furthermore, concentrations of fluoride in human plasma are much lower than fluoride concentrations, causing effects in cell cultures. In contrast, 21 of 23 recent epidemiological studies report an association between high fluoride exposure and reduced intelligence. The discrepancy between experimental and epidemiological evidence may be reconciled with deficiencies inherent in most of these epidemiological studies on a putative association between fluoride and intelligence, especially with respect to adequate consideration of potential confounding factors, e.g., socioeconomic status, residence, breast feeding, low birth weight, maternal intelligence, and exposure to other neurotoxic chemicals. In conclusion, based on the totality of currently available scientific evidence, the present review does not support the presumption that fluoride should be assessed as a human developmental neurotoxicant at the current exposure levels in Europe.

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“…Curcumin seems to inhibit lipid peroxidation of quinolinic acid and controls the production of cyanide-induced superoxide in the brain, suggesting the protective properties of curcumin. In addition, nicotine treatment increased lipid peroxidation and the levels of GSH, IL-1β , TNF-α, and Bax, while reducing Bcl-2, P-CREB, and BDNF levels in the hippocampus 29 . Curcumin has been shown to significantly improve spatial memory impairment induced by HIV-1 gp120 V3 in rats, but the electrophysiological mechanism remains unknown 30 .…”

Section: Discussionmentioning

confidence: 90%

Toxicological evaluation of the nicotine on CA1 and protective effects of curcuma longa: An experimental study

et al. 2019

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Introduction: Nicotine is the most important alkaloid compound in tobacco and is a major risk factor in the development of functional disorders of several organ systems. Some plants produce Curcuma longa (curcumin), which has antioxidant and neuro-protective properties. Methods: This study was designed to evaluate the therapeutic effects of curcumin against nicotine injury on the hippocampus CA1 region of rats. In this study, 48 male rats were randomly assigned to eight groups: Normal control (saline) group, Nicotine control group (0.5 mg/kg); Curcumin groups (10, 30, and 60 mg/kg) and Nicotine + Curcumin groups (10, 30, and 60 mg/kg). Treatments were administered intra-peritoneally daily for 28 days. Golgi staining technique investigated the number of dendritic spines. Cresyl violet staining method was used to determine the number of neurons in the hippocampal region CA1. Griess technique was assessed to determine serum nitrite oxide levels. Also, the ferric reducing/antioxidant power (FRAP) method was applied to determine the total antioxidant capacity. Results: Nicotine administration significantly increased the nitrite oxide level and decreased total antioxidant capacity. The number of neuronal dendritic spines, as well as neurons per se, also decreased, compared to the control group (p < 0.01). In all the members of the Curcumin and Nicotine + Curcumin groups, the number of neurons, neuronal dendritic spines and total antioxidant capacity increased significantly compared to the nicotine control group, while nitrite oxide level decreased significantly compared to the nicotine control group (p < 0.01). Conclusions: It seems that Curcumin administration improved hippocampal CA1 region injury in rats caused by Nicotine.

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Alterations in the memory of rat offspring exposed to low levels of fluoride during gestation and lactation: Involvement of the α7 nicotinic receptor and oxidative stress

Cited by 24 publications

References 63 publications

Effect of curcumin on hippocampus dentate gyrus injury induced by nicotine in rats

Effect of curcumin on hippocampus dentate gyrus injury induced by nicotine in rats

Toxicity of fluoride: critical evaluation of evidence for human developmental neurotoxicity in epidemiological studies, animal experiments and in vitro analyses

Toxicological evaluation of the nicotine on CA1 and protective effects of curcuma longa: An experimental study

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