Protective effect of methylene blue against copper oxide nanoparticle-induced neurobehavioral toxicity

Neuroprotective Assessment of Betaine against Copper Oxide Nanoparticle-Induced Neurotoxicity in the Brains of Albino Rats: A Histopathological, Neurochemical, and Molecular Investigation

“…In the open field test as depicted in Table 1, CuO-NPs intoxicated rats displayed a significant reduction in the locomotor and exploratory activity, as evidenced by a marked decline in the number of crossing squares and rearing activity compared to control. These results are in agreement with previous studies of Goma et al and Tohamy et al, 17,36 who used different treatment modalities to ameliorate CuO-NP toxicity such as methylene blue and nanocurcumin. However, administration of betaine was able to ameliorate the toxicity in betaine+ CuO-NP-treated rats by increasing the locomotor activity due to its antioxidant activity as reported in many studies.…”

“…The findings of this investigation revealed detrimental histopathological alterations in the cerebral cortex, cerebellar cortex, and hippocampus of group II that were exposed to CuO-NPs in comparison to those of the control group (GPI) and the group administered with betaine (GPVI). The aforementioned alterations can be depicted as follows: severe vascular congestion, subpial hemorrhage, and erythrocytic extravasation, which were in line with Goma et al 17 who orally treated 20 adult male albino rats for 14 days with CuO-NPs at a dose of 100 mg/kg. The observed vascular changes can be attributed to the breakdown of the BBB caused by the small dimensions of the CuO-NPs, enabling their passage over the BBB.…”

“…In addition, it has been observed that they are afflicted with specific neurodegenerative disorders . CuO-NPs toxicity causes elevation of several oxidative stress biomarkers − as well as histopathological alterations in vital organs, including the brain − and the liver. ,− The brain exhibits increased susceptibility to oxidative stress due to its elevated concentration of polyunsaturated fatty acids (PUFA) and limited presence of antioxidant enzymes in comparison to other organs inside the body . CuO-NPs possess the ability to traverse biological barriers, such as the blood-brain barrier (BBB), owing to their minuscule dimensions.…”

Boosting the therapy of glutamine-addiction glioblastoma by combining glutamine metabolism therapy with photo-enhanced chemodynamic therapy

“…S8,† CuCl 2 solution effectively inhibited the activity of GLUD1 and GPx1 proteins in U87 MG cells, and the treated cells displayed reduced red/green fluorescence compared with the untreated cells. The results demonstrated that copper ions could significantly inhibit the activity of the intracellular GPx1 protein, 54,55 and exposure to copper also caused a decrease in the mitochondrial dehydrogenase (ALDH2 and GLUD1) activity, 56 which could be the reason for reduced α-KG and fumarate in the cells treated with CS NPs.…”

HINT1 Is Involved in the Chronic Mild Stress Elicited Oxidative Stress and Apoptosis Through the PKC ε/ALDH-2/4HNE Pathway in Prefrontal Cortex of Rats

“…Mitochondrial aldehyde dehydrogenase-two (ALDH-2), which is enriched in brain, plays an important role in maintaining the function of mitochondria ( Xia et al, 2020 ), and prevents against OS and apoptosis ( Liu et al, 2017c ; Wang et al, 2017 ). The activation or suppression of ALDH-2 could be bi-directionally regulated via protein kinase C (PKC) ε phosphorylation in the brain, and also associated with metabolizing other biogenic aldehydes such as 4-hydroxynonenal (4HNE) or malondialdehyde (MDA) ( Li et al, 2017 ; Goma et al, 2021 ).…”