Curcumin protects against the oxidative damage induced by the pesticide parathion in the hippocampus of the rat brain

Canales-Aguirre, Alejandro A.; Gómez‐Pinedo, Ulises; Luquı́n, Sonia; Ramírez-Herrera, Mario Alberto; Mendoza-Magaña, María Luisa; Feria‐Velasco, Alfredo

doi:10.1179/1476830511y.0000000034

Cited by 39 publications

(21 citation statements)

References 23 publications

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“…However, few studies have investigated the histopathological effects of ATR exposure on the ultrastructure of the hippocampal neurons, and only one reported histopathological alternation to the hippocampus in response to ATR at 100 µg/kg BW, which included a significant reduction in the total number of neurons, perikaryal swelling, and astrocytic formations in the dentate gyrus of female mice [32]. Nonetheless, other pesticides, such as paraquat and parathion, are known to cause histopathological damage to the hippocampal neurons, including pyknosis, irregular arrangement, and apoptosis, which could lead to impairment of hippocampus-dependent learning and memory [33,34]. Another major finding of the electron microscopy analysis conducted in the present study was that the synaptic clefts in the ATR-treated groups were not as clear, as compared with the control group.…”

Section: Discussionmentioning

confidence: 99%

Developmental Exposure to Atrazine Impairs Spatial Memory and Downregulates the Hippocampal D1 Dopamine Receptor and cAMP-Dependent Signaling Pathway in Rats

et al. 2018

IJMS

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Atrazine (ATR) is a widely used herbicide that has been implicated as a neurotoxicant. Recent experimental evidence has implicated that ATR exposure also appears to have adverse effects on the hippocampus, which is a critical region for learning and memory. The aim of the present study was to investigate the effects of ATR toxicity on the hippocampus of developing rats. Postnatal day (PND) 28 male Sprague–Dawley (SD) rats received ATR by oral gavage at 10 or 100 mg/kg bodyweight (BW) for 30 consecutive days and were sacrificed at PND 90. Behavioral test results indicated that spatial learning and memory were affected by ATR treatment. Electron microscopy analysis showed that the ultrastructures of the hippocampus were altered in the ATR-treated groups, as compared to the control group. Additionally, ATR treatment impacted dopamine and D1 dopamine receptor (D1DR) contents through different mechanisms. Reduced mRNA and protein expression levels of factors involved in the cAMP-dependent signaling pathway were also detected. These results indicate that the developmental exposure of rats to ATR can damage the hippocampus and spatial memory, which might be related to the downregulation of expression levels of the D1DR and its downstream signaling pathway.

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Section: Discussionmentioning

confidence: 99%

Developmental Exposure to Atrazine Impairs Spatial Memory and Downregulates the Hippocampal D1 Dopamine Receptor and cAMP-Dependent Signaling Pathway in Rats

et al. 2018

IJMS

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“…These proteins reduce electrophiles and free radicals to less toxic intermediates whilst increasing the ability of the cell to repair any subsequent damage [1, 10, 15, 16]. In this regard, curcumin is able to induce protection and activate Nrf2-dependent protective responses in cell lines or animal models exposed to oxidative conditions [17, 18]. …”

Section: Introductionmentioning

confidence: 99%

Curcumin Pretreatment Induces Nrf2 and an Antioxidant Response and Prevents Hemin-Induced Toxicity in Primary Cultures of Cerebellar Granule Neurons of Rats

González-Reyes

Guzmán-Beltrán

Medina-Campos

et al. 2013

Oxidative Medicine and Cellular Longevity

148

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Curcumin is a bifunctional antioxidant derived from Curcuma longa. This study identifies curcumin as a neuroprotectant against hemin-induced damage in primary cultures of cerebellar granule neurons (CGNs) of rats. Hemin, the oxidized form of heme, is a highly reactive compound that induces cellular injury. Pretreatment of CGNs with 5–30 μM curcumin effectively increased by 2.3–4.9 fold heme oxygenase-1 (HO-1) expression and by 5.6–14.3-fold glutathione (GSH) levels. Moreover, 15 μM curcumin attenuated by 55% the increase in reactive oxygen species (ROS) production, by 94% the reduction of GSH/glutathione disulfide (GSSG) ratio, and by 49% the cell death induced by hemin. The inhibition of heme oxygenase system or GSH synthesis with tin mesoporphyrin and buthionine sulfoximine, respectively, suppressed the protective effect of curcumin against hemin-induced toxicity. These data strongly suggest that HO-1 and GSH play a major role in the protective effect of curcumin. Furthermore, it was found that 24 h of incubation with curcumin increases by 1.4-, 2.3-, and 5.2-fold the activity of glutathione reductase, glutathione S-transferase and superoxide dismutase, respectively. Additionally, it was found that curcumin was capable of inducing nuclear factor (erythroid-derived 2)-like 2 (Nrf2) translocation into the nucleus. These data suggest that the pretreatment with curcumin induces Nrf2 and an antioxidant response that may play an important role in the protective effect of this antioxidant against hemin-induced neuronal death.

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“…Curcumin is the yellow and bioactive component of turmeric with potent antioxidant (Canales-Aguirre et al, 2012) and neuroprotective activity (Mansouri et al, 2012). There is increasing evidence that curcumin could afford neuroprotection against oxidative stress-induced brain insult (Agrawal et al, 2012;Tiwari & Chopra, 2012).…”

Section: Introductionmentioning

confidence: 99%

Antiepileptogenic effect of curcumin on kainate-induced model of temporal lobe epilepsy

Kiasalari

Roghani

Khalili

et al. 2013

Pharmaceutical Biology

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Context: Temporal lobe epilepsy (TLE) is an intractable neurological disorder. Curcumin is the bioactive component of turmeric with anti-epileptic and neuroprotective potential. Objective: The beneficial effect of curcumin on the intrahippocampal kainate-induced model of TLE was investigated. Materials and methods: Rats were divided into sham, curcumin-pretreated sham, kainate and curcumin-pretreated kainate groups. The rat model of TLE was induced by unilateral intrahippocampal injection of 4 mg of kainate. Rats received curcumin p.o. at a dose of 100 mg/kg/d starting 1 week before the surgery. Seizure activity (SE) and oxidative stressrelated markers were measured. Furthermore, the Timm index for evaluation of mossy fiber sprouting (MFS) and number of Nissl-stained neurons were quantified. Results: All rats in the kainate group had SE, while 28.5% of rats showed seizures in the curcumin-pretreated kainate group. Malondialdehyde and nitrite and nitrate levels significantly increased in the kainate group (p50.01 and p50.05, respectively), and curcumin significantly lowered these parameters (p50.05). Superoxide dismutase activity significantly decreased in the kainate group (p50.05) and curcumin did not improve it. Rats in the kainate group showed a significant reduction of neurons in Cornu Ammonis 1 (CA1) (p50.05), CA3 (p50.005) and hilar (p50.01) regions, and curcumin significantly prevented these changes (p50.05-0.005). The Timm index significantly increased in the kainate group (p50.005), and curcumin significantly lowered this index (p50.01). Discussion and conclusion: Curcumin pretreatment can attenuate seizures, lower some oxidative stress markers, and prevent hippocampal neuronal loss and MFS in the kainate-induced model of TLE.

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Curcumin protects against the oxidative damage induced by the pesticide parathion in the hippocampus of the rat brain

Abstract: These data suggest that CUR may be an alternative to prevent neurodegenerative damage after pesticide exposure.

Cited by 39 publications

References 23 publications

Developmental Exposure to Atrazine Impairs Spatial Memory and Downregulates the Hippocampal D1 Dopamine Receptor and cAMP-Dependent Signaling Pathway in Rats

Developmental Exposure to Atrazine Impairs Spatial Memory and Downregulates the Hippocampal D1 Dopamine Receptor and cAMP-Dependent Signaling Pathway in Rats

Curcumin Pretreatment Induces Nrf2 and an Antioxidant Response and Prevents Hemin-Induced Toxicity in Primary Cultures of Cerebellar Granule Neurons of Rats

Antiepileptogenic effect of curcumin on kainate-induced model of temporal lobe epilepsy

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