Aug 2026· Environmental Toxicology· 0 citations· 74 references
Medicine
TL;DR
It is demonstrated that MAL induces hepatotoxicity by promoting oxidative stress, inflammation, and apoptosis, whereas morin exerts significant hepatoprotective effects, likely through modulation of antioxidant defense systems and apoptotic pathways.
Abstract
Malathion (MAL) is a widely used organophosphate pesticide associated with hepatotoxicity through oxidative stress and apoptosis. Morin, a naturally occurring flavonoid, exhibits potent antioxidant and anti-inflammatory properties. This study investigated oxidative stress, inflammatory, and apoptotic alterations induced by acute and subacute MAL exposure in rats and evaluated the potential protective effects of morin. Fifty 3-month-old male Sprague Dawley rats were randomly assigned to six groups: control, morin (200 mg/kg), subacute MAL (150 mg/kg), acute MAL (300 mg/kg), subacute MAL + morin, and acute MAL + morin. At the end of the experimental period, liver tissues and plasma samples were analyzed. Hepatic malondialdehyde (MDA) and glutathione (GSH) levels; catalase (CAT), glutathione peroxidase (GSH-Px), superoxide dismutase (SOD), and glutathione S-transferase (GST) activities; plasma aspartate aminotransferase (AST), alanine aminotransferase (ALT), and alkaline phosphatase (ALP) activities; and tissue acetylcholinesterase (AChE), butyrylcholinesterase (BChE), tumor necrosis factor-α (TNF-α), B-cell lymphoma 2 (Bcl-2), Bcl-2-associated X protein (Bax), Bax/Bcl-2 ratio and caspase-3 levels were determined. MAL exposure significantly increased MDA, TNF-α, Bax, Bax/Bcl-2 ratio, caspase-3, and liver enzyme activities, while decreasing GSH levels, antioxidant enzyme activities, AChE, BChE, and Bcl-2 levels (p < 0.001). Histopathological findings included hepatocellular swelling, focal necrosis, sinusoidal congestion, periportal infiltration, and bile duct proliferation, with more pronounced lesions in the subacute MAL group. Morin administration markedly attenuated biochemical alterations and improved histopathological damage. These findings demonstrate that MAL induces hepatotoxicity by promoting oxidative stress, inflammation, and apoptosis, whereas morin exerts significant hepatoprotective effects, likely through modulation of antioxidant defense systems and apoptotic pathways.
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, Ö. Hazman, Laçine Aksoy et al.· Animal Health Production and...· 0 citations
Cadmium (Cd) is a highly toxic heavy metal that accumulates primarily in the kidneys, where it induces oxidative stress, inflammation, and cellular damage. Cd exposure is a major environmental and occupational concern due to its persistence and bioaccumulative nature. Morin, a natural flavonoid abundant in various fruits and medicinal plants, possesses potent antioxidant and anti-inflammatory properties. However, its potential protective efficacy against Cd-induced nephrotoxicity has not been fully elucidated. This study aimed to evaluate the protective effects of Morin against Cd-induced oxidative and inflammatory damage in rat kidney tissue and to assess its association with oxidative stress and inflammatory responses. Fifty adult male Sprague-Dawley rats were randomly divided into five groups: Control, Cd (6.5 mg/kg, i.p.), Morin100+Cd (100 mg/kg Morin + Cd), Morin200+Cd (200 mg/kg Morin + Cd), and Morin200 (200 mg/kg Morin alone). Cadmium was administered intraperitoneally for 5 consecutive days, while Morin was given intragastrically one hour before Cd injection. Cadmium exposure significantly elevated malondialdehyde (MDA) levels and proinflammatory cytokines (TNF-α, IL-1β, IL-6, IFN-γ) while reducing the activities of antioxidant enzymes (SOD, CAT, GPx, GSH) and anti-inflammatory cytokines (IL-10, IL-4). Morin treatment, particularly at 200 mg/kg, markedly ameliorated these alterations by suppressing oxidative stress, restoring antioxidant enzyme activities, and modulating cytokine balance. These findings indicate that Morin exerts a strong nephroprotective effect against Cd-induced renal toxicity through attenuation of oxidative stress and inflammation, possibly associated with its antioxidant and anti-inflammatory properties. Therefore, Morin may represent a promising natural therapeutic candidate for the prevention of heavy metal-induced renal injury.
Burak Batuhan Laçin, Furkan Aykurt, S. Tekin et al.· Erciyes Üniversitesi Veterin...· 0 citations
Di-n-butyl phthalate (DBP), a widely used plasticizer, induces oxidative stress and neurotoxicity through the generation of reactive oxygen species. Ellagic acid (EA), a natural polyphenolic antioxidant, may counteract these effects. This study aimed to evaluate the protective role of EA against DBP-induced oxidative brain injury. Thirty-two male rats were randomly divided into four groups: Control, DBP, EA, and DBP+EA. DBP was administered orally at a dose of 500 mg/kg/day, while EA was given by gavage at 2 mg/kg/day for four weeks. Oxidative stress parameters, including thiobarbituric acid reactive substances (TBARS), reduced glutathione (GSH), superoxide dismutase (SOD), and catalase (CAT) activities were analyzed in brain tissue. DBP exposure significantly increased TBARS levels while decreasing GSH and SOD activities, indicating lipid peroxidation and antioxidant depletion. In contrast, CAT activity was elevated, suggesting a compensatory enzymatic response to excess hydrogen peroxide. EA treatment markedly attenuated oxidative damage by restoring GSH and SOD levels and normalizing CAT activity. These findings indicate that DBP disrupts redox homeostasis by inducing lipid peroxidation, while EA mitigates this effect through restoration of antioxidant defenses.
İdris Ayhan, Neşe Başak Türkmen, Demet Döndü Kasım et al.· Muğla Sıtkı Koçman Üniversit...· 0 citations
It is implied that resveratrol improves the antioxidant status of the body against diazinon toxicity, so it can improve renal function in the face of diazinon.
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
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.
Özge Darakcı Saltık, H. Balcı, Figen Güzelgül et al.· Yüksek İhtisas Üniversitesi...· 0 citations
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