Neurotoxic effects of environmental contaminants—measurements, mechanistic insight, and environmental relevance

Afsheen, Nadia; Rafique, Sadia; Rafeeq, Hamza; Irshad, Kanwal; Hussain, Altaf; Huma, Zille; Kumar, Vineet; Bilal, Muhammad; Aleya, Lotfi; Iqbal, Hafiz M.N.

doi:10.1007/s11356-022-22779-2

Cited by 6 publications

(3 citation statements)

References 113 publications

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“…Moreover, microglia, the predominant immune cells found in the brain, along with astrocytes and oligodendrocytes, albeit to a lesser degree, are linked to the degeneration of neurons in PD (Badanjak et al, 2021;Leyane et al, 2022) Specific endogenous proteins and environmental contaminants can induce microglia to become too active and generate ROS, which can be neurotoxic (Afsheen et al, 2022) A growing body of evidence suggests that activation of various enzymes, such as NOX2 in microglia, is neurotoxic not only by producing extracellular ROS that harm nearby neurons but also by commencing redox signaling in microglia that intensifies the pro-inflammatory response (Pajares et al, 2020;Begum et al, 2022) Therefore, reducing the harmful effects of oxidative stress in neurodegenerative disorders relies on discovering prospective therapeutics that can postpone the neurodegenerative process. In the coming years, neuroprotective interventions must focus on various pathogenic mechanisms, including neuroinflammation and mitochondrial dysfunction.…”

Section: Parkinson's Disease (Pd)mentioning

confidence: 99%

From imbalance to impairment: the central role of reactive oxygen species in oxidative stress-induced disorders and therapeutic exploration

Afzal,

Abdul Manap,

Attiq

et al. 2023

Front. Pharmacol.

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Increased production and buildup of reactive oxygen species (ROS) can lead to various health issues, including metabolic problems, cancers, and neurological conditions. Our bodies counteract ROS with biological antioxidants such as SOD, CAT, and GPx, which help prevent cellular damage. However, if there is an imbalance between ROS and these antioxidants, it can result in oxidative stress. This can cause genetic and epigenetic changes at the molecular level. This review delves into how ROS plays a role in disorders caused by oxidative stress. We also look at animal models used for researching ROS pathways. This study offers insights into the mechanism, pathology, epigenetic changes, and animal models to assist in drug development and disease understanding.

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Section: Parkinson's Disease (Pd)mentioning

confidence: 99%

From imbalance to impairment: the central role of reactive oxygen species in oxidative stress-induced disorders and therapeutic exploration

Afzal,

Abdul Manap,

Attiq

et al. 2023

Front. Pharmacol.

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“…Anhita Torkaman-Boutorabi et.al 2022 Parkinson's disease (PD) is a multifactorial movement illness that affects patients' capacity to move. It is caused by the nigrostriatal system's gradual degradation [126]. The aetiology and pathogenesis of Parkinson's disease have been discovered to be impacted by oxidative stress.…”

Section: Terpenoid Chemical Constituents Used As Parkinson Diseasementioning

confidence: 99%

Role of Terpenoids Active Ingredients Targeting for Neuroprotective Agents

Kashyap,

Kumar,

Rana

et al. 2023

J. Res. Appl. Sci. Biotechnol.

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Neuroinflammation is a characteristic sign of a wide variety of neurodegenerative diseases, including Alzheimer's and Parkinson's, amongst others. Microglia, which are native immune cells found in the brain, become activated very quickly in response to a brain infection or injury. When microglia become overactivated, their production of pro-inflammatory and cytotoxic chemicals can become unregulated and uncontrolled, which is the primary cause of neuroinflammation. Microglia are principally responsible for neuroinflammation. As a result, the investigation of novel approaches to reduce neuroinflammatory reactions is an essential component of neurodegenerative disease treatment. In the research of brain inflammation, bacterial lipopolysaccharide is frequently used. This compound is responsible for the initiation of a number of significant cellular processes that significantly contribute to the pathophysiology of neuroinflammation.

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“…Despite significant progress in toxicant research, data on the potential risks to brain cells are rather limited. In addition, research on the effects of neurotoxic compounds has focused primarily on animal models and/or clinical observations of human health (Afsheen et al, 2022).…”

Section: Introductionmentioning

confidence: 99%

Cypermethrin induces neurotoxicity via inhibition of glial cell viability and apoptosis initiation

Sukharenko,

Gasso

2022

TAVM

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The progress in agricultural productivity is accompanied by the increase in the global application of pesticides. Moreover, the number of different pesticides used is growing permanently all over the world. Several types of pesticides are effective tools to suppress the propagation of insects, bacteria, and fungi. However, they could correlate with toxicity for other non-targeted organisms including mammalian and humans. Neurotoxicity is considered to be the most detrimental effect of pesticides given the ecotoxicology studies of the environmental pollution consequences for the last decades. Exposure to neurotoxic pesticides can induce multiple harmful disturbances in the deregulation of vital molecular pathways, cellular response, and programmed cell death initiation as well as lead to a decline in the functioning of the central neural system (CNS). All of them are potent in inhibiting the adaptation mechanisms and viability of vertebrate populations. The pyrethroids are the most total used group of pesticides. This study of the neurotoxic effects of pyrethroids aimed to contribute to assessing the risk rate in the application of compromised chemicals in agriculture production. Glial cells are the prevailing population in the CNS. Measurement of the cytotoxic effect of pollutants can be assessed by their neurotoxicity in glial cell culture. In the present study, we detected glioma U251 cells' viability, oxidative stress indices, and a mitochondria-associated marker of apoptosis to evaluate the molecular mechanism of cypermethrin neurotoxicity. Obtained results have shown that 2 and 5 μg/ml doses of cypermethrin inhibited glioma U251 cell viability (p<0.05) and increased an oxidative stress level. Contrary, the dose of cypermethrin 1 μg/ml did not induce statistically significant both cell viability and oxidative stress. However, 2 and 5 μg/ml doses of cypermethrin exposure induced cytochrome C release to cytosol in a dose-dependent manner that is a marker of apoptosis initiation. Thus, the neurotoxic effect of pyrethroids can be mediated by the mitochondrial-dependent apoptotic pathway activation via cytochrome C release.

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Neurotoxic effects of environmental contaminants—measurements, mechanistic insight, and environmental relevance

Cited by 6 publications

References 113 publications

From imbalance to impairment: the central role of reactive oxygen species in oxidative stress-induced disorders and therapeutic exploration

From imbalance to impairment: the central role of reactive oxygen species in oxidative stress-induced disorders and therapeutic exploration

Role of Terpenoids Active Ingredients Targeting for Neuroprotective Agents

Cypermethrin induces neurotoxicity via inhibition of glial cell viability and apoptosis initiation

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