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<p><b>Background</b>: Alzheimer disease (AD) in animals is associated with increased levels of free radicals and damage to internal organs. We investigated male reproductive damage and lactate/cAMP/AK signaling pathway linkage in AlCl3-induced AD. <b>Methods</b>: Wistar rats were exposed to Al (10–50 mg/kg) in drinking water for two and four weeks (control groups received drinking water only). In the end, the rat’s blood was taken and serum levels of malondialdehyde (MDA), superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase (CAT) and sex steroid hormone (testosterone), gonadotropins and inflammatory factors (IL-1β and TNF-α), cortisol, and lactate were measured with immunosorbent assay (ELISA). The testicles and hippocampus (on ice) were dissected for histology and immunohistochemistry. The results were analyzed by ANOVA (α=0.05). <b>Findings</b>: Compared to the control, the rat receiving Al had a decrease in the serum levels of luteinizing hormone (LH), and testosterone with an increase in the level of follicle-stimulating hormone (FSH) without significant change in cortisol. Levels of IL-1β, TNF-α, MDA and lactate increased significantly, but a significant decrease occurred in antioxidant markers, especially in the 4-week period. The level of testosterone receptor in animals receiving Al had a decreasing trend. The hippocampus tissue had a decrease in neuronal population and the testes showed reduced germinal layer thickness, however, Leydig and Sertoli cells did not decrease and macrophage cells showed no infiltration. <b>Conclusion</b>: Al-induced AD in rats is not only associated with increased oxidative stress and inflammation, but also characterized by testicular damage and increased lactate levels as the end product of the cAMP/AK signaling pathway.</p>

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AlCl3-induced Alzheimer's in rats: linking oxidative stress, inflammation, and lactate production via the cAMP/AK signaling pathway

  • 期刊论文

  • 发表日期：

    2025年1月24日

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  • Roza Seifi,
  • Manizheh Karami,
  • Mohammadreza Jalali-Nadoushan

摘要

Background: Alzheimer disease (AD) in animals is associated with increased levels of free radicals and damage to internal organs. We investigated male reproductive damage and lactate/cAMP/AK signaling pathway linkage in AlCl3-induced AD. Methods: Wistar rats were exposed to Al (10–50 mg/kg) in drinking water for two and four weeks (control groups received drinking water only). In the end, the rat’s blood was taken and serum levels of malondialdehyde (MDA), superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase (CAT) and sex steroid hormone (testosterone), gonadotropins and inflammatory factors (IL-1β and TNF-α), cortisol, and lactate were measured with immunosorbent assay (ELISA). The testicles and hippocampus (on ice) were dissected for histology and immunohistochemistry. The results were analyzed by ANOVA (α=0.05). Findings: Compared to the control, the rat receiving Al had a decrease in the serum levels of luteinizing hormone (LH), and testosterone with an increase in the level of follicle-stimulating hormone (FSH) without significant change in cortisol. Levels of IL-1β, TNF-α, MDA and lactate increased significantly, but a significant decrease occurred in antioxidant markers, especially in the 4-week period. The level of testosterone receptor in animals receiving Al had a decreasing trend. The hippocampus tissue had a decrease in neuronal population and the testes showed reduced germinal layer thickness, however, Leydig and Sertoli cells did not decrease and macrophage cells showed no infiltration. Conclusion: Al-induced AD in rats is not only associated with increased oxidative stress and inflammation, but also characterized by testicular damage and increased lactate levels as the end product of the cAMP/AK signaling pathway.