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Your search keyword '"Aschner, Michael"' showing total 45 results
Start Over Author "Aschner, Michael" Journal biological trace element research
45 results on '"Aschner, Michael"'

24. Therapeutic Effects of Sodium Para-Aminosalicylic Acid on Cognitive Deficits and Activated ERK1/2-p90RSK/NF-κB Inflammatory Pathway in Pb-Exposed Rats.

Author

Lu, Li-li, Zhang, Yu-wen, Li, Zhao-cong, Fang, Yuan-yuan, Wang, Lei-lei, Zhao, Yue-song, Li, Shao-jun, Ou, Shi-yan, Aschner, Michael, and Jiang, Yue-ming

Abstract

Lead (Pb) is a toxic heavy metal and environmental pollutant that adversely affects the nervous system. However, effective therapeutic drugs for Pb-induced neurotoxicity have yet to be developed. In the present study, we investigated the ameliorative effect of sodium para-aminosalicylic acid (PAS-Na) on Pb-induced neurotoxicity. Male Sprague–Dawley rats were treated with (CH3COO)2 Pb•4H2O (6 mg/kg) for 4 weeks, followed by 3 weeks of PAS-Na (100, 200, and 300 mg/kg). The results showed that subacute Pb exposure significantly decreased rats body-weight gains and increased liver coefficient, and impaired spatial learning and memory. HE staining showed that Pb damaged the structure of the hippocampus. Moreover, Pb activated the ERK1/2-p90RSK/ NF-κB pathway concomitant with increased inflammatory cytokine IL-1β levels in rat hippocampus. PAS-Na reversed the Pb-induced increase in the liver coefficient as well as the learning and memory deficits. In addition, PAS-Na reduced the phosphorylation of ERK1/2, p90RSK and NF-κB p65, decreasing IL-1β levels in hippocampus. Our findings indicated that PAS-Na showed efficacy in reversing Pb-induced rats cognitive deficits and triggered an anti-inflammatory response. Thus, PAS-Na may be a promising therapy for treating Pb-induced neurotoxicity. [ABSTRACT FROM AUTHOR]

Published
2022
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45. Manganese Alters Rat Brain Amino Acids Levels.

Author

Santos, Dinamene, Batoreu, M., Almeida, Isabel, Ramos, Ruben, Sidoryk-Wegrzynowicz, M., Aschner, Michael, and Marreilha dos Santos, A.

Abstract

Manganese (Mn) is an essential element and it acts as a cofactor for a number of enzymatic reactions, including those involved in amino acid, lipid, protein, and carbohydrate metabolism. Excessive exposure to Mn can lead to poisoning, characterized by psychiatric disturbances and an extrapyramidal disorder. Mn-induced neuronal degeneration is associated with alterations in amino acids metabolism. In the present study, we analyzed whole rat brain amino acid content subsequent to four or eight intraperitoneal injections, with 25 mg MnCl/kg/day, at 48-h intervals. We noted a significant increase in glycine brain levels after four or eight Mn injections ( p < 0.05 and p < 0.01, respectively) and arginine also after four or eight injections ( p < 0.001). Significant increases were also noted in brain proline ( p < 0.01), cysteine ( p < 0.05), phenylalanine ( p < 0.01), and tyrosine ( p < 0.01) levels after eight Mn injections vs. the control group. These findings suggest that Mn-induced alterations in amino acid levels secondary to Mn affect the neurochemical milieu. [ABSTRACT FROM AUTHOR]

Published
2013
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