Protective effects of curcumin and Ganoderma lucidum on hippocampal damage caused by the organophosphate insecticide chlorpyrifos in the developing rat brain: Stereological, histopathological and immunohistochemical study

Eronat, Kübra; Sağir, Dilek

doi:10.1016/j.acthis.2020.151621

Cited by 12 publications

(11 citation statements)

References 49 publications

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“…CPF caused some remarkable histological aberrations in brain tissues. Similar observations were reported by [ 4 , 73 , 74 , 75 ]. However, supplementation with OLE largely restored normal histology.…”

Section: Discussionsupporting

confidence: 92%

Olive Leaf Extract Attenuates Chlorpyrifos-Induced Neuro- and Reproductive Toxicity in Male Albino Rats

Hassan

Salah

Fahmy

et al. 2022

Life

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Chlorpyrifos (CPF) is a common organophosphorus insecticide. It is associated with negative consequences such as neurotoxicity and reproductive injury. This study aimed to observe the ability of olive leaf extract to attenuate chlorpyrifos toxicity, which induced neuro- and reproductive toxicity in male albino rats. Olive leaf extract (OLE) exhibits potent antioxidant and antiapoptotic properties. Twenty-two mature male rats were divided into four groups: control (saline), CPF (9 mg/kg), OLE (150 mg/kg), and CPF + OLE. Treatment was administered orally for 80 days. The CPF significantly reduced serum sex hormones, sperm counts and motility, high oxidants (MDA), and depleted antioxidants (GSH, SOD, TAC) in the brain and testes homogenate; additionally, it decreased serum AChE and brain neurotransmitters, increased Bax, decreased Bcl-2, and boosted caspase-3 immune expression in neural and testicular cells. Immunological expression of Ki 67 in the cerebrum, cerebellum, choroid plexus, and hippocampus was reduced, and α-SMA in testicular tissue also decreased. Histopathological findings were consistent with the above impacts. OLE co-administration significantly normalized all these abnormalities. OLE showed significant protection against neural and reproductive damage caused by CPF.

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Section: Discussionsupporting

confidence: 92%

Olive Leaf Extract Attenuates Chlorpyrifos-Induced Neuro- and Reproductive Toxicity in Male Albino Rats

Hassan

Salah

Fahmy

et al. 2022

Life

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“…CPF functions as a neurotoxic by suppressing AchE, a membrane-bound enzyme essential for acetylcholine (Ach) metabolism at the neuro-muscular junctions and cholinergic synapses [ 34 ]. CPF inhibits AchE irreversibly by phosphorylating the enzyme’s serine OH group, leading to Ach buildup in the brain and hyperstimulation of the cholinergic nerve system, resulting in a variety of clinical disorders [ 35 ]. Along with the aforementioned, the current work affirmed that CPF induced neurotoxicity was elucidated by a substantial decrease in AchE levels in CPF-intoxicated rats compared to controls.…”

Section: Discussionmentioning

confidence: 99%

“…In addition to AchE suppression, other evidence proposed that excessive production of ROS and lipid peroxidation (LPO) are other mechanisms implicated in CPF-induced neuropathy [ 5 , 9 , 10 ]. ROS (hydroxyl radical, OH • ; hydrogen peroxide, H 2 O 2 ; superoxide anion, O 2 •− ) and reactive nitrogen species (nitric oxide, NO and peroxynitrite, ONOO − ) are reported to be invigorated during CPF intoxication as a result of exhaustion of the endogenous antioxidant molecules [ 5 , 7 , 35 ]. Verma et al [ 6 ] has documented alterations in the antioxidant system, including superoxide dismutase (SOD), catalase (CAT), and reduced glutathione (GSH) in CPF-intoxicated rats.…”

Section: Discussionmentioning

confidence: 99%

“…The cysteine residue of GSH provides a nucleophilic thiol that is paramount in the detoxification of electrophilic metabolites. Besides, GSH is important for the regeneration of the enzymatic antioxidants, GPx and glutathione-S-transferase (GST), and is required for maintaining cellular antioxidant competence [ 35 , 38 ].…”

Section: Discussionmentioning

confidence: 99%

“…•− ) and reactive nitrogen species (nitric oxide, NO and peroxynitrite, ONOO − ) are reported to be invigorated during CPF intoxication as a result of exhaustion of the endogenous antioxidant molecules [5,7,35]. Verma et al [6] has documented alterations in the antioxidant system, including superoxide dismutase (SOD), catalase (CAT), and reduced glutathione (GSH) in CPF-intoxicated rats.…”

Section: Discussionmentioning

confidence: 99%

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Antioxidant and Anti-Inflammatory Potential of Thymoquinone and Lycopene Mitigate the Chlorpyrifos-Induced Toxic Neuropathy

et al. 2021

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CPF (chlorpyrifos) is an organophosphate pesticide used in agricultural and veterinary applications. Our experiment aimed to explore the effects of thymoquinone (TQ) and/or lycopene (LP) against CPF-induced neurotoxicity. Wistar rats were categorized into seven groups: first group served as a control (corn oil only); second group, TQ (10 mg/kg); third group, LP (10 mg/kg); fourth group, CPF (10 mg/kg) and deemed as CPF toxic control; fifth group, TQ + CPF; sixth group, (LP + CPF); and seventh group, (TQ + LP + CPF). CPF intoxication inhibited acetylcholinesterase (AchE), decreased glutathione (GSH) content, and increased levels of malondialdehyde (MDA), an oxidative stress biomarker. Furthermore, CPF impaired the activity of antioxidant enzymes including superoxide dismutase (SOD) and catalase (CAT) along with enhancement of the level of inflammatory mediators such as tumor necrosis factor-α (TNF-α), interleukin (IL)-6, and IL-1β. CPF evoked apoptosis in brain tissue. TQ or LP treatment of CPF-intoxicated rats greatly improved AchE activity, oxidative state, inflammatory responses, and cell death. Co-administration of TQ and LP showed better restoration than their sole treatment. In conclusion, TQ or LP supplementation may alleviate CPF-induced neuronal injury, most likely due to TQ or LPs’ antioxidant, anti-inflammatory, and anti-apoptotic effects.

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Evaluating the effect of ginsenoside Rg1 on CPF‐induced brain injury in mice via PI3k/AKT pathway

Liu

Pei

Chen

et al. 2023

J Biochem & Molecular Tox

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Organophosphorus pesticides (OPs) have long been used extensively on agricultural land and can lead to significant improvements in crop yields. Due to occupational exposure, humans are exposed to pesticides through dermal contact, inhalation, and ingestion. The effects of OPs on the organism are currently studied for their effects on livers, kidneys, hearts, blood indicators, neurotoxicity, and teratogenic, carcinogenic, and mutagenic effects, while studies in the direction of brain tissue damage have not been reported in detail. Previous reports have confirmed that ginsenoside Rg1 is a prominent and representative tetracyclic triterpenoid derivative rich in ginseng and has good neuroprotective activity. Considering that, the aim of this study was to establish a mouse model of brain tissue injury by using the OP-type pesticide chlorpyrifos (CPF) and to explore the therapeutic effects and possible molecular mechanisms of Rg1. Mice in the experimental group were pre-protected with Rg1 by gavage for 1 week, and brain tissue damage was induced using CPF (5 mg/kg for 1 week) to assess the effect of Rg1 (80 and 160 mg/kg for 3 weeks) in alleviating brain damage. Morris water maze and histopathological analysis were performed to assess cognitive function and pathological changes in the mouse brain, respectively. Protein expression levels of Bax, Bcl-2, Caspase-3, Cl-Cas-3, Caspase-9, Cl-Cas-9, phosphoinositide 3-kinase (PI3K), phosphorylated-PI3K, protein kinase B (AKT), and phosphorylated-AKT were quantified by protein blotting analysis. Rg1 obviously restored CPF-induced oxidative stress damage in mouse brain tissue, increased the levels of antioxidant parameters (total superoxide dismutase, total antioxidative capacity, and glutathione) in the brain, and significantly reduced the overexpression of apoptosis-related proteins induced by CPF. At the same time, Rg1 also markedly attenuated the histopathological changes in the brain induced by CPF exposure. Mechanistically, Rg1 could effectively activate the phosphorylation of PI3K/AKT. Furthermore, molecular docking studies revealed a stronger binding capacity between Rg1 and PI3K. Rg1 attenuated neurobehavioural alterations and reduced lipid peroxidation in the mouse brain to a great extent. Apart from that, Rg1 administration improved brain histopathology in CPF-induced rats. All results suggest that ginsenoside Rg1 has potential antioxidant effects on CPF-induced

show abstract

Protective effects of curcumin and Ganoderma lucidum on hippocampal damage caused by the organophosphate insecticide chlorpyrifos in the developing rat brain: Stereological, histopathological and immunohistochemical study

Cited by 12 publications

References 49 publications

Olive Leaf Extract Attenuates Chlorpyrifos-Induced Neuro- and Reproductive Toxicity in Male Albino Rats

Olive Leaf Extract Attenuates Chlorpyrifos-Induced Neuro- and Reproductive Toxicity in Male Albino Rats

Antioxidant and Anti-Inflammatory Potential of Thymoquinone and Lycopene Mitigate the Chlorpyrifos-Induced Toxic Neuropathy

Evaluating the effect of ginsenoside Rg1 on CPF‐induced brain injury in mice via PI3k/AKT pathway

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