Neuronal Apoptosis and Imbalance of Neurotransmitters Induced by Acetamiprid in Rats

Gasmi, Salim; Chafaa, Smail; Lakroun, Zhora; Rouabhi, Rachid; Touahria, Chouaib; Kebieche, Mohamed; Soulimani, Rachid

doi:10.1007/s13530-019-0417-1

Cited by 12 publications

(11 citation statements)

References 27 publications

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“…[ 44 ] The toxicity of ACMP is associated with disruption of the activity of AChE, dopamine, serotonin, and adrenaline inside the brain. [ 45 ] In the present study, ACMP‐exposed rats showed increased activity of AChE in all three brain regions. The varying degree of AChE elevation in different regions suggested a peculiar pattern of functional cholinergic interaction within different brain areas.…”

Section: Discussionsupporting

confidence: 56%

Neuroprotective potential of berberine against acetamiprid induced toxicity in rats: Implication of oxidative stress, mitochondrial alterations, and structural changes in brain regions

Phogat

Singh

Malik

et al. 2023

J Biochem & Molecular Tox

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Acetamiprid (ACMP) is an extensively used neonicotinoid pesticide to control sucking and chewing insects and is known to cause nontarget toxicity. The present study aimed to evaluate the ameliorative potential of berberine (BBR)—a polyphenolic alkaloid‐ on ACMP‐induced oxidative stress, mitochondrial dysfunctioning, and structural changes in different rat brain regions. The male Wistar rats were divided into four groups, that is, control, BBR‐treated (150 mg/kg b.wt), ACMP‐exposed (21.7 mg/kg b.wt) and BBR + ACMP co‐treated; and were dosed intragastrically for 21 consecutive days. Results of the biochemical analysis showed that BBR significantly ameliorated ACMP‐induced oxidative stress by decreasing lipid peroxidation and protein oxidation along with a marked increase in endogenous antioxidants and lowered AChE activity in rat brain regions. Inside mitochondria, BBR significantly attenuated the toxic effects of ACMP by increasing the activity of mitochondrial complexes. Findings of polymerase chain reaction also demonstrated the modulatory effects of BBR against ACMP‐mediated downregulation of ND1, ND2, COX1, and COX4 subunits of mitochondrial complexes. The histopathological and ultrastructural examination also validated the biochemical and transcriptional alterations following toxicity of ACMP exposure and the protective potential of BBR against ACMP‐induced neurotoxicity. Thus, the present study indicates the promising ameliorative potential of BBR against ACMP‐induced neurotoxicity via its antioxidative and modulatory activities.

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Section: Discussionsupporting

confidence: 56%

Neuroprotective potential of berberine against acetamiprid induced toxicity in rats: Implication of oxidative stress, mitochondrial alterations, and structural changes in brain regions

Phogat

Singh

Malik

et al. 2023

J Biochem & Molecular Tox

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“… 66 Also, 5-HT levels were decreased in the IMI group, which could be attributed to the destruction of brain regions with a high density of serotonergic neurons due to oxidative damage induced by IMI administration. 68 Interestingly, our study shows a significant reduction in AchE activity due to IMI exposure. Our results were found to be in accordance with Bhardwaj et al, 69 and Vohra et al 70 Brain AchE inhibition suggested that several regions in the brain are subjected to significant damage.…”

Section: Discussionmentioning

confidence: 52%

“…Similarly to the synthesis of GABA, as oxidative stress gets enhanced, DA synthesis is also inhibited, which is mediated by the reduction of tyrosine hydroxylase, the synthesizing enzyme, and the rate-limiting step of DA production through the formation of 3-nitrotyrosine by peroxynitrite, which may downregulate the activity of tyrosine hydroxylase . Also, 5-HT levels were decreased in the IMI group, which could be attributed to the destruction of brain regions with a high density of serotonergic neurons due to oxidative damage induced by IMI administration . Interestingly, our study shows a significant reduction in AchE activity due to IMI exposure.…”

Section: Discussionmentioning

confidence: 56%

Potential Mechanisms of Imidacloprid-Induced Neurotoxicity in Adult Rats with Attempts on Protection Using Origanum majorana L. Oil/Extract: In Vivo and In Silico Studies

et al. 2023

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Imidacloprid (IMI) insecticide is rapidly metabolized in mammals and contributes to neurotoxicity via the blocking of nicotinic acetylcholine receptors, as in insects. Origanum majorana retains its great antioxidant potential in both fresh and dry forms. No data is available on the neuroprotective effect of this plant in laboratory animals. In this context, aerial parts of O. majorana were used to prepare the essential oil (OMO) and methanol extract (OME). The potential neuroprotective impact of both OMO and OME against IMI-induced neurotoxicity in rats was explored. Forty-two rats were divided into 6 groups, with 7 rats in each one. Rats were daily administered the oral treatments: normal saline, OMO, OME, IMI, IMI + OMO, and IMI + OME. Our results revealed the identification of 55 components in O. majorana essential oil, most belonging to the oxygenated and hydrocarbon monoterpenoid group. Moreover, 37 constituents were identified in the methanol extract, mostly phenolics. The potent neurotoxic effect of IMI on rats was confirmed by neurobehavioral and neuropathological alterations and a reduction of both acetylcholine esterase (AchE) activity and dopamine (DA), serotonin (5HT), and γ-aminobutyric acid (GABA) levels in the brain. Exposure of rats to IMI elevates the malondialdehyde (MDA) levels and reduces the antioxidant capacity. IMI could upregulate the transcription levels of nuclear factor-κB (NF-κB), interleukin-1 β (IL-1β), and tumor necrosis factor (TNF-α) genes and express strong caspase-3 and inducible nitric oxide synthase (iNOS) immunostaining in most examined brain areas. On the other hand, rats coadministered OMO or OME with IMI showed a marked improvement in all of the studied toxicological parameters. In conclusion, cotreatment of O. majorana extracts with IMI can protect against IMI neurotoxicity via their potent antioxidant, anti-inflammatory, and anti-apoptotic effects. Thus, we recommend a daily intake of O. majorana to protect against insecticide’s oxidative stress-mediated neuroinflammatory stress and apoptosis. The molecular docking study of linalool, rosmarinic acid, γ-terpene, and terpene-4-ol justify the observed normalization of the elevated iNOS and TNF-α levels induced after exposure to IMI.

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“…Accordingly, it was proposed by (Gasmi et al, 2019;Yisa et al, 2023) that the GST enzyme's activity contributed to the detoxi cation of steroids in the studied species, either separately or in combination. Therefore, in order to improve toxicity endpoint forecasts and revisions, particularly for aquatic environmental risk assessment, the pollution pro le databases for both hormones need to be expanded.…”

Section: Mitochondrial Respiration Discussionmentioning

confidence: 97%

Assessment of two steroid hormones Progestin and estrogen on cellular model Paramecium: oxidative stress, Mitochondrial swelling and kinetic.

Zouaoui,

Rouabhi,

Bouzenzana

et al. 2023

Preprint

Self Cite

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Synthetic steroids like progestin and estrogen, which are frequently present in contraceptive pills, alter behavior, physiology, and biochemistry in life beings. Although, the harmful effects of neosynthesized products are widely researched, there are no reports on their individual or mixture uses. Therefore, this study is to evaluate the effects of each component alone and in combination on Paramecia, a freshwater protozoan, at low relevant ambient concentrations in a ratio that is comparable to that of most recommended by doctors. The cells kinetics test was used to evaluate the acute toxicity of these two steroids, individually and their mixture after 24 and 48 hours. Furthermore, the consequences of oxidative stress were investigated over a duration of 120 hours. While the mixture largely impeded motility, immobility was concentration-dependent, Progestin is less impacts than Estrogen. Oxidative stress responses demonstrated a substantial drop in GSH contents and SOD, CAT activity, as well as an increase in MDA levels and GST activity in treated groups relative to the control (p < 0.01). These results imply that while these two steroids caused a generation of reactive oxygen species (ROS) in Paramecium, this result was confirmed by the mitochondrial assessments respiration and swelling that explain the amount of cellular number reduction.

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Neuronal Apoptosis and Imbalance of Neurotransmitters Induced by Acetamiprid in Rats

Cited by 12 publications

References 27 publications

Neuroprotective potential of berberine against acetamiprid induced toxicity in rats: Implication of oxidative stress, mitochondrial alterations, and structural changes in brain regions

Neuroprotective potential of berberine against acetamiprid induced toxicity in rats: Implication of oxidative stress, mitochondrial alterations, and structural changes in brain regions

Potential Mechanisms of Imidacloprid-Induced Neurotoxicity in Adult Rats with Attempts on Protection Using Origanum majorana L. Oil/Extract: In Vivo and In Silico Studies

Assessment of two steroid hormones Progestin and estrogen on cellular model Paramecium: oxidative stress, Mitochondrial swelling and kinetic.

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