Jul 2026· Toxicology and industrial health· pp.
7482337261467527
· 0 citations· 53 references
Medicine
TL;DR
Investigating the dose-dependent toxicity of AlP on biochemical biomarkers, antioxidant defense responses, and histological changes in rat liver and kidneys found sub-acute AlP exposure caused dose-dependent liver and kidney toxicity, high doses induced pronounced damage, and low doses showed mild or minimal effects.
Abstract
Aluminium phosphide (AlP) is a well-known toxic pesticide, but its dose-dependent toxicity and the distinction between safe and harmful exposure levels remain poorly established. Thus, the present study aimed to investigate the dose-dependent toxicity of AlP on biochemical biomarkers, antioxidant defense responses, and histological changes in rat liver and kidneys. Adult male Wistar rats were treated orally with increasing AlP doses (0.38, 0.58, and 1.15 mg/kg body weight, corresponding to LD50/30, LD50/20, and LD50/10, respectively) for 4 weeks. Results revealed a marked increase in body weight, serum levels of AST (aspartate aminotransferase), ALT (alanine aminotransferase), and PAL (alkaline phosphatase), and levels of urea, creatinine, and malondialdehyde (MDA) of treated rats as compared with controls. However, glutathione content and enzymatic activity of catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx), and glutathione S-transferase (GST) in liver and kidney tissue were significantly decreased compared with controls. These biochemical changes following AlP treatment also mirrored hepatic and renal histopathological observations, showing dose-dependent tissue alterations, with a more pronounced effect in the higher AlP dose-treated rats. Conclusively, sub-acute AlP exposure caused dose-dependent liver and kidney toxicity, high doses induced pronounced damage, and low doses showed mild or minimal effects.
Organophosphate pesticides, particularly malathion, are widely used in agriculture but pose severe toxicity risks to non-target organisms through acetylcholinesterase (AChE) enzyme inhibition and the induction of oxidative stress. This study investigated the potential protective effects of safranal, a primary bioactive component of saffron (Crocus sativus L.) known for its antioxidant and anti-inflammatory properties, against malathion-induced systemic and tissue-specific toxicity. Experimental groups were evaluated by measuring malondialdehyde (MDA), nitric oxide (NO), glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), and GPx (glutathione peroxidase) levels, alongside AChE enzyme activity in the blood, liver, kidney, and brain tissues. The findings demonstrated that malathion exposure caused profound toxicity characterized by severe AChE inhibition, accelerated lipid peroxidation, elevated NO levels, and a critical depletion of both enzymatic and non-enzymatic antioxidant defenses across all analyzed matrices. Conversely, safranal administration served as an effective therapeutic intervention. It mitigated oxidative damage, limited the exhaustion of key antioxidant enzymes by reducing reactive oxygen species, and supported the preservation of AChE functionality. Notably, safranal’s protective efficacy exhibited tissue-dependent variations; while it significantly attenuated oxidative stress markers and preserved cellular viability in the plasma, liver, and renal matrices, it demonstrated limited protective capacity in brain tissue under the current experimental conditions. In conclusion, safranal represents a promising bioactive countermeasure against organophosphate-induced systemic injury. However, further research is warranted to elucidate its precise transport mechanisms and potential limitations in crossing the blood-brain barrier.
Ahmet Büyükben, Ömer Hazman, Laçine Aksoy et al.· Animal Health Production and...· 0 citations
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
Özge Darakcı Saltık, H. Balcı, Figen Güzelgül et al.· Yüksek İhtisas Üniversitesi...· 0 citations
Rosmarinus officinalis extract may exert protective effects against MTX-induced hepatorenal injury through antioxidant and anti-inflammatory mechanisms, however, further studies are required to confirm these effects and validate their therapeutic potential.
Lana Muhammed, Nadia Salih· Open Veterinary Journal· 0 citations
BackgroundFood additives such as monosodium glutamate (MSG), sodium benzoate (SB), and Sunset Yellow (SY) are widely consumed and have been linked to adverse hepatic effects. However, the available evidence is largely derived from in vitro or single-additive studies, with limited comparative in vivo data integrating biochemical and histopathological outcomes under uniform experimental conditions.ObjectiveThis study compared the hepatotoxic effects of MSG, SB, and SY in a Wistar rat model to address gaps in controlled in vivo evidence on multiple food additives.MethodsSixteen healthy Wistar rats were randomly assigned to four groups. The control group received a standard diet, while Groups II–IV received MSG, SB, and SY respectively. Hepatotoxicity was assessed by measuring serum activities of aspartate aminotransferase, alanine aminotransferase, and alkaline phosphatase, together with histopathological examination of liver tissue.ResultsThe MSG and SB significantly increased aspartate aminotransferase (AST) and alkaline phosphatase (ALP) levels compared with controls (p < 0.05), indicating hepatocellular and cholestatic injury. Sunset Yellow did not significantly alter ALT levels (p = 0.074) but showed mild histopathological changes.ConclusionBoth MSG and SB exhibited greater hepatotoxic effects than SY in Wistar rats. These findings highlight the need for routine safety re-evaluation of commonly consumed food additives, strengthened regulatory oversight, and further long-term studies to inform evidence-based public health policies.Rwanda J Med Health Sci 2026;9(2):327-341
Ude Ugomma, Okorie Nnaemeka, Uzor Simon et al.· Rwanda Journal of Medicine a...· 0 citations
ABSTRACTThe present study aimed to investigate the protective effects of selenium (SE) against enrofloxacin (ENRO) induced liver damage through oxidative stress, inflammation, and autophagy pathways. Rats were divided into four groups: control (received physiological saline via oral gavage and intraperitoneal (i.p.) injection for 7 days); selenium (1 mg/kg, oral, 7 days); enrofloxacin (150 mg/kg, i.p., 7 days); and enrofloxacin (150 mg/kg, i.p., 7 days) + selenium (1 mg/kg, oral, 7 days). In liver tissues, oxidative stress markers including malondialdehyde (MDA), reduced glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) were measured. Additionally, nuclear factor kappa B (NF-κB), interleukin-1 beta (IL-1β), tumor necrosis factor-alpha (TNF-α), and Beclin-1 expression were analyzed to evaluate inflammatory and autophagic responses ENRO administration increased NF-κB, IL-1β, TNF-α, and Beclin-1 expression together with elevated MDA levels, while decreasing GSH levels and SOD, CAT, and GPx activities. These alterations indicate increased lipid peroxidation, inflammation, and autophagy. These findings indicate that ENRO disrupts antioxidant defense systems and promotes inflammatory and autophagy-related responses in liver tissue. SE supplementation reduced MDA levels, enhanced GSH levels and antioxidant enzyme activities, and significantly ameliorated these alterations by suppressing NF-κB, IL-1β, TNF-α, and Beclin-1 expression. In conclusion, SE was found to exert hepatoprotective effects against ENRO induced liver injury by reducing lipid peroxidation, strengthening antioxidant defense systems, and regulating inflammatory and autophagic responses.
A. Genç, F. Kandemir, E. Dalkılınç et al.· Veterinary Sciences and Prac...· 0 citations