TL;DR
Co-administration of CoQ10 mitigates MSG-induced nephrotoxicity and oxidative stress, suggesting its potential therapeutic application in protecting renal function against dietary MSG exposure.
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
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
Overall, chrysin demonstrates potent protective potential against PFOA-induced liver injury and may serve as a promising therapeutic candidate for environmental toxin-associated hepatotoxicity.
Pyrrolizidine alkaloids (PAs) are plant toxins of increasing concern due to their toxic and carcinogenic properties. While the hepatotoxic effects of PAs are well established, limited information is available regarding oxidative stress–related damage in extrahepatic tissues. This study aimed to determine alterations associated with oxidative stress and apoptosis in plasma, lung, and kidney tissues following acute and subacute exposure to monocrotaline (MCT) in mice. Thirty male BALB/c mice were randomly assigned to three groups: control, acute exposure, and subacute exposure. The control group received saline, the acute exposure group received a single dose of 120 mg/kg MCT, and the subacute exposure group received the same dose three times at five-day intervals. Plasma, lung, and kidney samples were collected for biochemical and molecular analyses. Total antioxidant status (TAS) and total oxidant status (TOS) levels were measured using a spectrophotometric method in plasma and tissue samples. Furthermore, plasma total thiol (TT), native thiol (NT), and disulfide (DD) levels were determined. The expression levels of BAX and BCL-2 genes in lung and kidney tissues were assessed using qPCR. MCT exposure significantly increased plasma TOS and oxidative stress index (OSI) levels in both exposure groups compared with the control group (P < 0.05). In lung tissue, TOS and OSI levels were significantly elevated, whereas TAS showed a non-significant increase. In kidney tissue, only TOS levels were significantly increased. Plasma NT levels were significantly decreased (P < 0.001), while DD levels were significantly increased (P < 0.05). In addition, BAX expression increased and the BCL-2/BAX ratio decreased in lung and kidney tissues, indicating a shift toward a pro-apoptotic state. In conclusion, MCT induces marked oxidative stress in lung and kidney tissues and promotes apoptotic signaling, suggesting that PA toxicity involves systemic and extrahepatic organ damage through oxidative imbalance.
Background: Naturally derived compounds with antioxidant and hepatoprotective potential are being actively explored. 2′,6′-Dihydroxyacetophenone (DHDA), a phenolic compound, has shown antioxidant properties, but its role in diabetic liver injury remains inadequately investigated. Aim and objectives: This study aimed to assess the protective effects of DHDA on diabetes-induced liver injury in a rat model. Materials and methods: Acute toxicity was conducted by using mice. Diabetes was induced in Wistar rats using streptozotocin (STZ) following nicotinamide(NA) pretreatment. Animals were divided into four groups: normal control, diabetic control, DHDA at dose of 30 mg/kg, and DHDA at dose 60 mg/kg. DHDA was administered orally for three weeks. Fasting blood glucose (FBG), body weight, food intake and, water intake were evaluated. In addition, the biochemical parameters, in-Vitro antioxidant and the histopathology of liver were analyzed. Result: 300 mg/kg is the safe dose of DHDA. DHDA significantly reduced FBG and glycated haemoglobin (HbA1c) levels in diabetic rats. Elevated liver enzymes and oxidative stress markers were markedly attenuated, while endogenous antioxidant defences were restored, particularly at dose of 60 mg/kg. In vitro assays confirmed dose-dependent free radical scavenging activity. Histopathological examination showed notable improvement in hepatic architecture. Conclusion: DHDA exhibits significant antihyperglycaemic, antioxidant, and hepatoprotective effects in diabetic rats, highlighting its potential as a therapeutic candidate for diabetes-associated liver injury.
