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Background <p>Lead (Pb) is a persistent environmental toxicant that induces oxidative stress, disrupts antioxidant defenses, and causes cellular damage with effects that can persist across generations. This study uses <i>Drosophila melanogaster</i> to examine transgenerational oxidative and antioxidant dysregulation following maternal lead exposure.</p> Methods <p>Wild-type <i>Drosophila melanogaster</i> (W<sup>1118</sup>) were maintained under controlled laboratory conditions on a standard cornmeal diet. In a randomized experimental design, parental flies (F0) were assigned to a control or a lead-exposed group. They received either a normal diet or one with 500&#xa0;ppm lead acetate for 20&#xa0;days. Transgenerational lineages (F1–F3) were produced through controlled crosses, with only maternal lead exposure transmitted. All offspring were reared on a lead-free diet. Oxidative stress was evaluated by measuring SOD, CAT, GSH, vitamins A, C, and E, and MDA using standard protocols. Expression of CAT and SOD1 was also assessed. Data were analyzed by one-way ANOVA followed by Tukey’s post hoc test and presented as mean ± SD.</p> Results <p>Maternal lead (Pb) exposure in <i>D. melanogaster</i> caused pronounced transgenerational oxidative stress, significantly affecting both enzymatic and non-enzymatic antioxidant defenses across four generations (F0–F3). In the F0 generation, direct exposure to Pb led to sharp reductions in GSH, vitamins A, C, and E, and suppressed CAT and SOD activities, while MDA levels were elevated, indicating enhanced lipid peroxidation (<i>p</i> &lt; 0.05). These disruptions persisted in F1 and F2 progeny reared on a lead-free diet, with antioxidant molecules and enzyme activities remaining depleted and CAT and SOD1 mRNA downregulated. Recovery trends varied: in F1 and F2, females began to recover GSH and vitamin A earlier than males, while by F3, GSH and vitamin A levels returned to control values in most groups. However, SOD, CAT, vitamin C, vitamin E, and MDA levels remained significantly altered in both sexes in F3, indicating partial recovery and continued impairment of certain antioxidant pathways.</p> Conclusion <p>Maternal lead exposure produced persistent transgenerational redox imbalance, marked by sex-specific recovery trajectories and enduring disruption of crucial antioxidant defenses.</p>

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Transgenerational effects of maternal lead exposure on oxidative stress and antioxidant defense mechanisms in Drosophila melanogaster

  • 期刊论文

  • 发表日期：

    2026年7月24日

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  • Abduljalil Muhammad Mode,
  • Isah Musa Fakai,
  • Mustapha Umar Imam,
  • Aminu Argungu Umar

摘要

Background

Lead (Pb) is a persistent environmental toxicant that induces oxidative stress, disrupts antioxidant defenses, and causes cellular damage with effects that can persist across generations. This study uses Drosophila melanogaster to examine transgenerational oxidative and antioxidant dysregulation following maternal lead exposure.

Methods

Wild-type Drosophila melanogaster (W1118) were maintained under controlled laboratory conditions on a standard cornmeal diet. In a randomized experimental design, parental flies (F0) were assigned to a control or a lead-exposed group. They received either a normal diet or one with 500 ppm lead acetate for 20 days. Transgenerational lineages (F1–F3) were produced through controlled crosses, with only maternal lead exposure transmitted. All offspring were reared on a lead-free diet. Oxidative stress was evaluated by measuring SOD, CAT, GSH, vitamins A, C, and E, and MDA using standard protocols. Expression of CAT and SOD1 was also assessed. Data were analyzed by one-way ANOVA followed by Tukey’s post hoc test and presented as mean ± SD.

Results

Maternal lead (Pb) exposure in D. melanogaster caused pronounced transgenerational oxidative stress, significantly affecting both enzymatic and non-enzymatic antioxidant defenses across four generations (F0–F3). In the F0 generation, direct exposure to Pb led to sharp reductions in GSH, vitamins A, C, and E, and suppressed CAT and SOD activities, while MDA levels were elevated, indicating enhanced lipid peroxidation (p < 0.05). These disruptions persisted in F1 and F2 progeny reared on a lead-free diet, with antioxidant molecules and enzyme activities remaining depleted and CAT and SOD1 mRNA downregulated. Recovery trends varied: in F1 and F2, females began to recover GSH and vitamin A earlier than males, while by F3, GSH and vitamin A levels returned to control values in most groups. However, SOD, CAT, vitamin C, vitamin E, and MDA levels remained significantly altered in both sexes in F3, indicating partial recovery and continued impairment of certain antioxidant pathways.

Conclusion

Maternal lead exposure produced persistent transgenerational redox imbalance, marked by sex-specific recovery trajectories and enduring disruption of crucial antioxidant defenses.