Neuroprotective Effects of Naringin Against Lead Acetate‐Induced Oxidative Stress and Neurotoxicity in Wistar Rats

Lead acetate (LA) exposure induces oxidative stress and neurotoxicity, leading to behavioral, biochemical, and histopathological alterations. Naringin, a natural flavonoid with potent antioxidant properties, has shown promise in ameliorating such damage. This study investigates the protective effects of naringin at different doses against LA-induced neurotoxicity in wistar rats. Thirty adult male wistar rats were randomly assigned to five groups (n = 6 each). Group I served as the control, receiving distilled water (2 mL/kg/day). Group II was administered LA (100 mg/kg/day) to induce neurotoxicity. Groups III, IV, and V were co-treated with LA and either N-acetylcysteine (NAC) (150 mg/kg/day), naringin low dose (50 mg/kg/day), or naringin high dose (100 mg/kg/day), respectively, for 28 days. At the end of the 28-day treatment period, blood and brain tissues were collected for biochemical assays. Apoptotic marker caspase-3 expression, oxidative stress markers such as malondialdehyde (MDA), catalase (CAT), and superoxide dismutase (SOD) levels were measured in serum and brain homogenates. Behavioral assessments were conducted using the elevated plus maze (EPM). Histopathological studies of brain tissues were also performed with a special focus on the hippocampus. The study highlights the neuroprotective effects of NAC and naringin against LA-induced neurotoxicity in wistar rats. LA exposure caused increased caspase-3 expression, elevated MDA levels, reduced antioxidant enzyme activities (CAT and SOD), and heightened anxiety-like behavior. NAC and high-dose naringin effectively mitigated these effects, restoring oxidative balance, improving behavior, and reducing neuronal damage. Histopathology confirmed significant neuroprotection with NAC and high-dose naringin, highlighting naringin's dose-dependent efficacy as a potential therapeutic agent comparable to NAC for lead-induced neurotoxicity. Naringin demonstrated dose-dependent neuroprotective effects against LA-induced neurotoxicity by improving antioxidant defenses, reducing oxidative stress, and preserving neuronal integrity. These findings support the therapeutic potential of naringin in managing neurotoxic conditions.

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Journal
Chemistry & Biodiversity
Published
2026-04-01
DOI
https://doi.org/10.1002/cbdv.202502291
Primary Topic
Heavy Metal Exposure and Toxicity
Type
article
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article

Neuroprotective Effects of Naringin Against Lead Acetate‐Induced Oxidative Stress and Neurotoxicity in Wistar Rats

Yuvaraj Maria Francis, Sankaran Ponnusamy Kasirajan, Nivetha Rajendiran, Indra Neel Pulidindi et al.
Chemistry & Biodiversity
Heavy Metal Exposure and Toxicity
article

Neuroprotective Effects of Naringin Against Lead Acetate‐Induced Oxidative Stress and Neurotoxicity in Wistar Rats

Yuvaraj Maria Francis, Sankaran Ponnusamy Kasirajan, Nivetha Rajendiran, Indra Neel Pulidindi, Senthilkumar Sivanesan, A. Sairam Kishore, Havila Hasini S, Meivelu Moovendhan
article en

Abstract

Lead acetate (LA) exposure induces oxidative stress and neurotoxicity, leading to behavioral, biochemical, and histopathological alterations. Naringin, a natural flavonoid with potent antioxidant properties, has shown promise in ameliorating such damage. This study investigates the protective effects of naringin at different doses against LA-induced neurotoxicity in wistar rats. Thirty adult male wistar rats were randomly assigned to five groups (n = 6 each). Group I served as the control, receiving distilled water (2 mL/kg/day). Group II was administered LA (100 mg/kg/day) to induce neurotoxicity. Groups III, IV, and V were co-treated with LA and either N-acetylcysteine (NAC) (150 mg/kg/day), naringin low dose (50 mg/kg/day), or naringin high dose (100 mg/kg/day), respectively, for 28 days. At the end of the 28-day treatment period, blood and brain tissues were collected for biochemical assays. Apoptotic marker caspase-3 expression, oxidative stress markers such as malondialdehyde (MDA), catalase (CAT), and superoxide dismutase (SOD) levels were measured in serum and brain homogenates. Behavioral assessments were conducted using the elevated plus maze (EPM). Histopathological studies of brain tissues were also performed with a special focus on the hippocampus. The study highlights the neuroprotective effects of NAC and naringin against LA-induced neurotoxicity in wistar rats. LA exposure caused increased caspase-3 expression, elevated MDA levels, reduced antioxidant enzyme activities (CAT and SOD), and heightened anxiety-like behavior. NAC and high-dose naringin effectively mitigated these effects, restoring oxidative balance, improving behavior, and reducing neuronal damage. Histopathology confirmed significant neuroprotection with NAC and high-dose naringin, highlighting naringin's dose-dependent efficacy as a potential therapeutic agent comparable to NAC for lead-induced neurotoxicity. Naringin demonstrated dose-dependent neuroprotective effects against LA-induced neurotoxicity by improving antioxidant defenses, reducing oxidative stress, and preserving neuronal integrity. These findings support the therapeutic potential of naringin in managing neurotoxic conditions.

Chemistry & BiodiversityVol. 23(4)
SRM University, Andhra Pradesh (IN), Apollo Institute of Medical Sciences & Research (IN), All India Institute of Medical Sciences (IN), Saveetha University (IN)
Clean water and sanitation
Openalex Percentile: Top 28%
Heavy Metal Exposure and Toxicity
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