2026· Yüksek İhtisas Üniversitesi Sağlık Bilimleri Dergisi· 0 citations
TL;DR
This study provides the first demonstration that asiatic acid exerts robust systemic antioxidative, hepatoprotective, and neuroprotective effects against CPF-induced toxicity, highlighting AA’s therapeutic potential for mitigating organophosphate pesticide poisoning.
Abstract
ABSTRACT
Introduction: Chlorpyrifos (CPF), one of the most widely used organophosphorus (OP) insecticides, exerts its toxic effects in part by inducing oxidative stress. Despite increasing recognition of natural antioxidants as potential countermeasures, the efficacy of asiatic acid (AA), a bioactive triterpenoid from Centella asiatica, against CPF-induced toxicity remains unexplored. This study aimed to investigate the protective effects of AA against CPF-incuded toxicity model in rats by analyzing biochemical and histological parameters in serum, liver, and brain tissues.
Material and Methods: Adult male Sprague Dawley rats (n=30) were randomly divided into five groups: control, CPF (279 mg/kg, subcutaneously), and three AA-pretreated groups (35, 70, and 140 mg/kg, per os) for 14 days prior to CPF exposure. Oxidative stress markers [malondialdehyde (MDA), advanced oxidation protein products (AOPP)] and antioxidant enzymes [superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx)] were measured in serum, liver, and brain. Histopathological and immunohistochemical analyses assessed tissue injury and apoptotic responses.
Results: AA administration significantly attenuated CPF-induced oxidative damage and restored antioxidant defenses in a dose-dependent manner. Histopathological analyses confirmed that AA mitigated hepatic and neuronal damage and preserved tissue architecture. Immunohistochemistry revealed that AA suppressed CPF-induced upregulation of the pro-apoptotic protein Bcl-2-associated X protein (Bax), indicating reduced apoptosis.
Conclusion: This study provides the first demonstration that AA exerts robust systemic antioxidative, hepatoprotective, and neuroprotective effects against CPF-induced toxicity. These findings highlight AA’s therapeutic potential for mitigating organophosphate pesticide poisoning, warranting further translational research.
Keywords: Asiatic acid, chlorpyrifos, hepatoprotection, neuroprotection, organophosphate toxicity, oxidative stress
Background:
Acrylamide (AC) is a highly reactive carbonyl compound widely used in industrial processes, having oxidative stress, neurotoxicity, and genotoxicity properties. Vinpocetine has been reported to exhibit neuroprotective, antioxidant, and anti-inflammatory properties.
Aim:
The study aims to evaluate vinpocetine’s protective effects in mitigating AC-induced toxicity in male albino rats.
Methods:
In the current research, 24 rats were used, arranged into 4 groups as follows: normal untreated group, Vinpo. group (5 mg/kg b.wt), AC group (38.27 mg/kg b.wt), Vinpo. + AC group (received Vinpo. and after one hour received a dose of AC). At the end of the experimental period, blood samples and brain specimens were collected from each rat to assess hematological and biochemical parameters and to conduct histopathological and immunohistochemical analyses.
Results:
AC administration caused a marked reduction in hematological parameters, reduced glutathione (GSH), superoxide dismutase (SOD), and brain-derived neurotrophic factor (BDNF). Also resulted in a marked reduction in key neurotransmitters (serotonin, dopamine, and acetylcholine (ACH)) as an indicator for oxidative stress and toxicity. Lipid peroxidation markers, like malondialdehyde (MDA), increase as an indicator of oxidative injury. The histological structural abnormalities and enhancement in the level of cleaved caspase-3 indicated the damage in brain tissues.
Conclusion:
Vinpocetine administration ameliorated hematological disturbances, oxidative damage, and histological alterations resulting from AC administration. These findings suggest that vinpocetine has a protective action against AC-induced neural damage.
M. El-Maksoud, E. Shaheen· Open Journal of Physiology a...· 0 citations
Potassium bromate (KBrO₃) is a potent oxidizing agent that induces oxidative stress and hepatic injury. This study investigated the protective effects of flavonoids extracted from Solanum aethiopicum leaves against KBrO₃-induced alterations in liver function, antioxidant status, and lipid profile in Wistar rats. Thirty rats were randomly assigned to six groups (n = 5): normal control, S. aethiopicum flavonoids (500 mg/kg), KBrO₃ (50 mg/kg), KBrO₃ + flavonoids (250 mg/kg), and KBrO₃ + flavonoids (500 mg/kg). At the end of the treatment period, serum liver function indices, antioxidant enzymes were determined using standard biochemical methods. Potassium bromate significantly (P < 0.05) reduced serum total protein, albumin, globulin, glutathione peroxidase (GPx), superoxide dismutase (SOD), and catalase (CAT), while significantly increasing alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), total bilirubin, malondialdehyde (MDA). Administration of S. aethiopicum flavonoids significantly reversed these alterations in a dose-dependent manner, with the 500 mg/kg dose showing greater protective effects than the 250 mg/kg dose. The flavonoid extract restored antioxidant enzyme activities, improved liver synthetic and excretory functions. These findings demonstrate that flavonoids extracted from Solanum aethiopicum leaves possess significant hepatoprotective, antioxidant properties against potassium bromate-induced toxicity. The observed protective effects are likely mediated through free radical scavenging, preservation of hepatocyte membrane integrity, and enhancement of endogenous antioxidant defenses. Solanum aethiopicum flavonoids therefore represent a promising natural therapeutic candidate for the prevention and management of oxidative stress-mediated liver dysfunction and associated metabolic disturbances.
Keywords: Hepatoprotective, antioxidants, flavonoids, Solanum aethiopicum, potassium bromate.
Okon Victoria Edem, Agabi Martina· IDOSR JOURNAL OF BIOCHEMISTR...· 0 citations
Dichlorvos is an organophosphate insecticide widely used in domestic and agricultural settings, and exposure is associated with significant toxicological effects, largely mediated by oxidative stress. This study evaluated the protective effects of the flavonoids quercetin and naringin against dichlorvos-induced subacute toxicity in male Wistar rats. Eighty male albino rats were randomly allocated into eight groups (n = 10); negative control (water), positive (vehicle) control (Dimethyl sulfoxide (DMSO)), Dichlorvos (8mg/kg BW), Dichlorvos recovery, Dichlorvos + naringin, Dichlorvos + quercetin, quercetin only, naringin only, and orally treated for 28 days. At the end of the experimental period, plasma, red blood cells, liver, and brain samples were collected for biochemical analyses. Activities of superoxide dismutase (SOD), catalase (CAT), and glutathione S-transferase (GST) were determined spectrophotometrically. Subacute dichlorvos (28-day) exposure caused significant reductions in SOD, CAT, and GST activities across all examined tissues, reflecting impaired antioxidant defense and increased oxidative stress. Coadministration of quercetin or naringin significantly attenuated these alterations, with enzyme activities approaching control levels. Quercetin showed greater protective efficacy in liver and brain tissues, whereas naringin exerted comparatively stronger effects in plasma and red blood cells, indicating tissue-specific antioxidant responses. Overall, the findings demonstrate that quercetin and naringin effectively protect against dichlorvos-induced subacute toxicity by modulating endogenous antioxidant enzymes, supporting the potential use of dietary flavonoids as adjunct protective agents against organophosphate toxicity.
A. Wusu, L. D. Adeleke, R. Kanmodi et al.· The Scientific World Journal· 0 citations
S. aethiopicum leaf extract protected against potassium bromate-induced hepatic dysfunction and inflammatory disturbances, supporting its potential as a natural hepatoprotective and immunomodulatory agent.
Okon Victoria Edem, Idam Benedict Umagu, I. Nnah· IAA Journal of Biological Sc...· 0 citations
Background: Pesticides like metribuzin are environmental pollutants that induce toxicity and oxidative stress in organisms. Methods: This study evaluates the protective role of Pulicaria odora extract against metribuzin-induced toxicity in Wistar rats. The leaves of P. odora were extracted using methanol-water (70:30, v/v), yielding phenolic (2.77 mg GAE/g) and flavonoid (0.77 mg QE/g) contents. Its antioxidant capacity, assessed by 2,2-diphenyl-1-picrylhydrazyl (DPPH) and ferric reducing antioxidant power (FRAP) assays. Result: Rats treated with metribuzin (13.2 mg/kg for 36 days) exhibited significant activity, including weight loss, altered hematological parameters and elevated hepatic (GPT, GOT) and renal (urea, creatinine) biomarkers. Co-administration of P. odora extract (34.2 mg/kg) significantly reversed these effects, restoring biomarkers and alleviating hepatic and renal toxicity by reducing transaminases, urea, creatinine, cholesterol and triglycerides. The extract’s antioxidant properties, attributed to its polyphenolic content, mitigated oxidative stress and stabilized cellular functions without adverse behavioral effects. This study highlights P. odora potential as a natural agent against herbicide-induced toxicity. Its bioactive compounds and mechanisms warrant further investigation, alongside exploring therapeutic applications in other Pulicaria species.
A. Benmahammed, A. Basli, F. Bouleknafet et al.· Indian Journal of Animal Res...· 0 citations
It is indicated that combining papaya, neem, and garlic extracts may provide greater hepatoprotection than administering the individual extracts against DEN-induced liver injury, and supports further mechanistic and preclinical evaluation of this polyherbal formulation before its potential therapeutic application in liver-disease management.
Egeonu Us, Umaru I. J., Izam Ed et al.· African Journal of Clinical...· 0 citations
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