ArticleBiological trace element research2026
Eucalyptol alleviates lead-induced nephrotoxicity in rats by suppressing oxidative stress, inflammation, and apoptosis, and enhancing the Nrf2/HO-1 signaling pathway.
Article in Biological trace element research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- β-caryophyllene attenuates lead acetate-induced hepatotoxicity through regulation of oxidative stress, inflammation, and PI3K/AKT/mTOR signaling.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Neuroprotective effect of L-borneol on acrylamide-induced neurotoxicity in the rat hippocampus: biochemical, molecular, histological, and behavioral approach.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Eucalyptol alleviates lead-induced nephrotoxicity in rats by suppressing oxidative stress, inflammation, and apoptosis, and enhancing the Nrf2/HO-1 signaling pathway.Biological trace element research · 2026Article
- Extraction process and antioxidant and antimicrobial activities of total flavonoids from Broussonetia papyrifera leaves.Scientific reports · 2025Article
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Abstract
Lead exposure is a significant factor in the development of chronic kidney disease. This study examined the effects of the monoterpene eucalyptol on nephrotoxicity induced by lead acetate in adult male Wistar rats. The animals were divided into four groups: Control, Eucalyptol, Lead, and Lead-Eucalyptol. Over 14 days, lead acetate (25 mg/kg) and eucalyptol (100 mg/kg) were administered via gavage. The results showed that eucalyptol reduced the levels of malondialdehyde in the kidneys of rats exposed to lead acetate (p < 0.05). It also increased levels of glutathione (p < 0.05) and enhanced the activities of the enzymes superoxide dismutase (p < 0.05) and glutathione peroxidase (p < 0.01). Likewise, eucalyptol reduced the expression of proinflammatory cytokines, including tumor necrosis factor-α (p < 0.01), interleukin (IL)-1 beta (p < 0.001), and IL-6 (p < 0.001) as well as Bax (p < 0.001) and caspase-3 (p < 0.001), while increasing the expression of Bcl2 (p < 0.01). It elevated the expression of nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) (p < 0.001), thereby preventing histopathological damage. Moreover, treatment with eucalyptol resulted in a reduction in serum creatinine and blood urea nitrogen levels in rats exposed to lead acetate (p < 0.001). We concluded that eucalyptol mitigates lead-induced nephrotoxicity by inhibiting oxidative stress, inflammation, and apoptosis. The renoprotective effects of eucalyptol appear to be mediated by the stimulation of the Nrf2/HO-1 signaling pathway. Therefore, eucalyptol may represent a promising option for reducing lead-induced toxicity.
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