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Background <p>Environmental exposure to heavy metals such as manganese (Mn) is associated with reproductive toxicity, particularly in females. Mn-induced ovarian dysfunction involves oxidative stress, hormonal imbalance, inflammation, and disruption of steroidogenesis. Lauric acid (LA) and levodopa (LD) are bioactive compounds with known antioxidant and anti-inflammatory properties. This study investigated the protective effects of LA and LD against Mn-induced ovarian toxicity in female BALB/c mice.</p> Methods <p>Thirty female BALB/c mice were randomly assigned to five groups (<i>n</i> = 6 per group): control, Mn-only, Mn + LA, Mn + LD, and Mn + LA + LD. Treatments were administered orally for 45 days. Biochemical assays and ELISA were used to evaluate ovarian oxidative stress markers (GSH and MDA), reproductive hormones (progesterone, estradiol, FSH, and LH), proinflammatory interleukins (IL-8-like cytokine, IL-12, IL-15, and IL-18), and the activities of key steroidogenic enzymes (3β-HSD1, 11β-HSD1, and 17β-HSD1). The data were analysed via one-way ANOVA followed by Tukey’s post hoc test (<i>p</i> &lt; 0.05).</p> Results <p>Mn exposure significantly increased oxidative stress and inflammatory cytokines while disrupting hormonal profiles and steroidogenic enzyme activity. Treatment with LA or LD independently alleviated these changes. Notably, coadministration of LA and LD enhanced protection by restoring oxidative balance, reducing proinflammatory interleukins, and normalizing steroid hormone levels and hydroxysteroid dehydrogenase activities.</p> Conclusions <p>Lauric acid and levodopa attenuate Mn-induced ovarian toxicity through antioxidant, anti-inflammatory, and steroidogenic regulatory mechanisms. The combined treatment offers synergistic benefits, suggesting a potential therapeutic strategy for mitigating heavy metal-induced reproductive dysfunction.</p>

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Lauric acid and levodopa attenuate manganese-induced ovarian toxicity in balb/c mice via antioxidative, anti-inflammatory, and steroidogenic pathways

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年10月31日

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  • Olumayowa Kolawole Idowu,
  • Monsurat Eniola Abdulgafar,
  • Adebusola Zainab Sogbesan,
  • Grace Ayobami Fajemidagba,
  • Abddullahi Abiodun Mohammed,
  • Tope Gafar Atere

摘要

Background

Environmental exposure to heavy metals such as manganese (Mn) is associated with reproductive toxicity, particularly in females. Mn-induced ovarian dysfunction involves oxidative stress, hormonal imbalance, inflammation, and disruption of steroidogenesis. Lauric acid (LA) and levodopa (LD) are bioactive compounds with known antioxidant and anti-inflammatory properties. This study investigated the protective effects of LA and LD against Mn-induced ovarian toxicity in female BALB/c mice.

Methods

Thirty female BALB/c mice were randomly assigned to five groups (n = 6 per group): control, Mn-only, Mn + LA, Mn + LD, and Mn + LA + LD. Treatments were administered orally for 45 days. Biochemical assays and ELISA were used to evaluate ovarian oxidative stress markers (GSH and MDA), reproductive hormones (progesterone, estradiol, FSH, and LH), proinflammatory interleukins (IL-8-like cytokine, IL-12, IL-15, and IL-18), and the activities of key steroidogenic enzymes (3β-HSD1, 11β-HSD1, and 17β-HSD1). The data were analysed via one-way ANOVA followed by Tukey’s post hoc test (p < 0.05).

Results

Mn exposure significantly increased oxidative stress and inflammatory cytokines while disrupting hormonal profiles and steroidogenic enzyme activity. Treatment with LA or LD independently alleviated these changes. Notably, coadministration of LA and LD enhanced protection by restoring oxidative balance, reducing proinflammatory interleukins, and normalizing steroid hormone levels and hydroxysteroid dehydrogenase activities.

Conclusions

Lauric acid and levodopa attenuate Mn-induced ovarian toxicity through antioxidant, anti-inflammatory, and steroidogenic regulatory mechanisms. The combined treatment offers synergistic benefits, suggesting a potential therapeutic strategy for mitigating heavy metal-induced reproductive dysfunction.