Shielding the Lungs: Nanocurcumin's Protective Role in Aluminum Phosphide-Induced Oxidative and Apoptotic Damage in rats

El-Din, Shimaa S.; Zaki, Sherif M.; Abdel-Fatah, Gaber H.; Medhat, Engy; Abd Algaleel, Waleed A.

doi:10.21608/eajbsc.2025.445538

Shielding the Lungs: Nanocurcumin's Protective Role in Aluminum Phosphide-Induced Oxidative and Apoptotic Damage in rats

Document Type : Original Article

Authors

¹ Department of Medical Biochemistry and Molecular biology, Faculty of Medicine, Cairo University, Egypt.

² Department of Physiological Sciences, MBBS program, Fakeeh College for Medical Sciences, Jeddah, Saudi Arabia.

³ Department of Anatomy and Embryology, Faculty of Medicine, Beni-Suef University, Egypt.

⁴ Department of Anatomy and Embryology, Faculty of Medicine, Cairo University, Egypt.

10.21608/eajbsc.2025.445538

Abstract

Aluminum phosphide (AlP) is a very dangerous pesticide that gives off phosphine gas (PH3), which causes oxidative stress, lipid peroxidation, and mitochondrial dysfunction, especially in lung tissue. This results in inflammation, apoptosis, and severe pulmonary damage. Due to the absence of an effective antidote, alternative therapeutic strategies are urgently needed. This research investigates how nanocurcumin (NCU) can protect against lung damage caused by AlP by changing the oxidative stress and apoptosis pathways. Thirty-two rats were divided into four groups: Control, NCU-only, AlP, and AlP +NCU. We analyzed the lung tissue histologically and immunohistochemically. We evaluated the relative gene expression of Nrf2, SOD, CAT, PCNA, BAX, and BCL2 via real-time PCR. Quantitative image analysis was applied for histopathological scoring.
Results illustrated that exposure to AlP caused noticeable changes in tissue structure, such as inflammation, thickened walls between air sacs, and swelling of blood vessels. AlP-treated lungs significantly upregulated Caspase-3 and PCNA. AlP lowered the levels of SOD and CAT proteins and raised the BAX/BCL2 ratio, showing that it caused oxidative stress and enhanced apoptosis. NCU administration significantly reversed these effects, improving lung histology, reducing apoptosis markers, restoring antioxidant enzyme expression, and lowering the BAX/BCL2 ratio by 85% compared to the AlP group. Given its potent antioxidant and anti-apoptotic effects, NCU may represent a promising adjunct in future clinical detoxification protocols for aluminum phosphide poisoning. However, advancing this to clinical practice requires further investigation about dose optimization and pharmacokinetic studies to ensure safety and efficacy.

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