Bioremediation: A favorable perspective to eliminate heavy metals from polluted soil

Kaur, Sukhchain; Midha, Tushar; Verma, Harkomal; Muduli, Rasmi Ranjan; Dutta, Oyindril; Saini, Omprakash; Prakash, Richa; Sharma, S.; Mantha, Anil K.; Dhiman, Monisha

doi:10.1016/b978-0-323-96113-4.00030-5

Cited by 7 publications

(1 citation statement)

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“…It is also a significant factor in a number of neurodegenerative diseases, including Parkinson's disease (PD) and AD. [108][109][110] According to reports, oxidative stress is a precursor to early AD events and is a major player in the development of NFTs (through destabilizing MTs by restricting tau's ability to bind to them), and Aβ induced oxidative stress responses in AD. [2,108,[111][112][113] The main source of oxidative stress is mitochondria, due to the obvious inevitable electron leakage that occurs during electron transfer.…”

Section: Oxidative Stress and Mitochondrial Dysfunction Associated Wi...mentioning

confidence: 99%

Implications of organophosphate pesticides on brain cells and their contribution toward progression of Alzheimer's disease

Yadav,

Kaur,

Yadav

et al. 2024

J Biochem & Molecular Tox

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The most widespread neurodegenerative disorder, Alzheimer's disease (AD) is marked by severe behavioral abnormalities, cognitive and functional impairments. It is inextricably linked with the deposition of amyloid β (Aβ) plaques and tau protein in the brain. Loss of white matter, neurons, synapses, and reactive microgliosis are also frequently observed in patients of AD. Although the causative mechanisms behind the neuropathological alterations in AD are not fully understood, they are likely influenced by hereditary and environmental factors. The etiology and pathogenesis of AD are significantly influenced by the cells of the central nervous system, namely, glial cells and neurons, which are directly engaged in the transmission of electrical signals and the processing of information. Emerging evidence suggests that exposure to organophosphate pesticides (OPPs) can trigger inflammatory responses in glial cells, leading to various cascades of events that contribute to neuroinflammation, neuronal damage, and ultimately, AD pathogenesis. Furthermore, there are striking similarities between the biomarkers associated with AD and OPPs, including neuroinflammation, oxidative stress, dysregulation of microRNA, and accumulation of toxic protein aggregates, such as amyloid β. These shared markers suggest a potential mechanistic link between OPP exposure and AD pathology. In this review, we attempt to address the role of OPPs on altered cell physiology of the brain cells leading to neuroinflammation, mitochondrial dysfunction, and oxidative stress linked with AD pathogenesis.

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