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Background <p>Methamphetamine (METH) is a potent psychostimulant with neurotoxic effects, while exposure to light-at-night (LAN) disrupts circadian rhythms and contributes to neuronal stress. Both are independently associated with oxidative damage and cognitive impairment, yet their combined effects on critical brain regions like the hippocampus and prefrontal cortex remain understudied. This study assessed the oxidative and histopathological alterations in the hippocampus and prefrontal cortex of Wistar rats following combined exposure to METH and LAN.</p> Methods <p>Twenty-eight adult male Wistar rats were divided into four groups (<i>n</i> = 7): Group A (Control), Group B (LAN only), Group C (METH only), and Group D (LAN + METH). METH (2&#xa0;mg/kg body weight) was administered intraperitoneally for 21 days to Groups C and D. For LAN exposure, rats in Groups B and D were subjected to continuous light during the usual dark cycle (18:00 to 06:00) throughout the experimental period. At the end of the study, brain tissues were collected for oxidative stress assays (MDA, SOD, GSH, CAT, and GSH-Px) and histological evaluation.</p> Results <p>In the hippocampus, MDA levels showed a non-significant increase across groups, while GSH significantly decreased in Groups B, C, and D. SOD decreased in Groups B and C but significantly increased in Group D. CAT activity decreased non-significantly in Groups B and D and significantly in Group C. In the prefrontal cortex, MDA significantly increased in all treatment groups, with a corresponding reduction in antioxidant enzyme levels, particularly GSH and GSH-Px. Histological analysis revealed mild pyknotic cells in LAN-only groups, moderate degeneration in METH-only groups, and extensive neuronal damage such as pyknosis, vacuolations, and disrupted lamination in the combined exposure group for both brain regions.</p> Conclusion <p>Combined METH and LAN exposure causes more severe oxidative stress and neurodegeneration in the hippocampus and prefrontal cortex than individual exposures. This was reflected in higher MDA levels, reduced antioxidant enzyme activities (SOD, CAT, GSH, and GSH-Px), and clear signs of neuronal degeneration, including pyknotic cells, vacuolations, and disorganized cortical layers in both the hippocampus and prefrontal cortex. The findings suggest that exposure to both METH and environmental stressors can work together to worsen oxidative imbalance and neuronal damage.</p> Clinical trial number <p>Not applicable.</p>

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Oxidative and histopathological changes in the hippocampus and prefrontal cortex following light-at-night and methamphetamine exposure

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年1月8日

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  • Smart Ikechukwu Mbagwu,
  • Usende Ifukibot Levi,
  • Ndubuisi Paris Obi,
  • Francis Elochukwu Chinwuba,
  • Clinton Onyekachi Anokwa,
  • Usende Ephraim Utopejit

摘要

Background

Methamphetamine (METH) is a potent psychostimulant with neurotoxic effects, while exposure to light-at-night (LAN) disrupts circadian rhythms and contributes to neuronal stress. Both are independently associated with oxidative damage and cognitive impairment, yet their combined effects on critical brain regions like the hippocampus and prefrontal cortex remain understudied. This study assessed the oxidative and histopathological alterations in the hippocampus and prefrontal cortex of Wistar rats following combined exposure to METH and LAN.

Methods

Twenty-eight adult male Wistar rats were divided into four groups (n = 7): Group A (Control), Group B (LAN only), Group C (METH only), and Group D (LAN + METH). METH (2 mg/kg body weight) was administered intraperitoneally for 21 days to Groups C and D. For LAN exposure, rats in Groups B and D were subjected to continuous light during the usual dark cycle (18:00 to 06:00) throughout the experimental period. At the end of the study, brain tissues were collected for oxidative stress assays (MDA, SOD, GSH, CAT, and GSH-Px) and histological evaluation.

Results

In the hippocampus, MDA levels showed a non-significant increase across groups, while GSH significantly decreased in Groups B, C, and D. SOD decreased in Groups B and C but significantly increased in Group D. CAT activity decreased non-significantly in Groups B and D and significantly in Group C. In the prefrontal cortex, MDA significantly increased in all treatment groups, with a corresponding reduction in antioxidant enzyme levels, particularly GSH and GSH-Px. Histological analysis revealed mild pyknotic cells in LAN-only groups, moderate degeneration in METH-only groups, and extensive neuronal damage such as pyknosis, vacuolations, and disrupted lamination in the combined exposure group for both brain regions.

Conclusion

Combined METH and LAN exposure causes more severe oxidative stress and neurodegeneration in the hippocampus and prefrontal cortex than individual exposures. This was reflected in higher MDA levels, reduced antioxidant enzyme activities (SOD, CAT, GSH, and GSH-Px), and clear signs of neuronal degeneration, including pyknotic cells, vacuolations, and disorganized cortical layers in both the hippocampus and prefrontal cortex. The findings suggest that exposure to both METH and environmental stressors can work together to worsen oxidative imbalance and neuronal damage.

Clinical trial number

Not applicable.