ArticleDaru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences2026
The paradoxical protective effect of malnutrition in acetaminophen-induced liver injury.
Article in Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundMalnutrition is believed to aggravate drug-induced liver injury (DILI). However, the relationship between protein malnutrition (PMN) and acetaminophen (APAP)-induced liver injury (AILI) remains unclear, particularly in low and middle income countries (LMIC) where PMN is common.
objectiveThis study aimed to investigate the role of PMN on AILI in female BALB/c mice. METHODOLOGY: PMN was induced in 15 week old female BALB/c mice by feeding a low protein diet (LPD, 10% protein) after weaning, while control mice received a normal diet (ND, 18% protein). Initially, APAP-induced lethality was assessed at different doses. Subsequently, mice were challenged with a single oral dose of APAP (300 mg/kg) to evaluate liver injury markers, oxidative stress, inflammatory cytokines, CYP2E1 expression and activity, histopathology, PCNA expression, and pharmacokinetic (PK) parameters.
resultsAt a single oral dose of 500 mg/kg, APAP-induced lethality was high in the LPD group (3/4). Reducing the dose to 400 mg/kg abolished lethality in the LPD group (0/6) but not in the ND group (4/6). At 300 mg/kg, lethality was absent in both groups. Liver injury assessed by ALT, AST, and ALP levels was greater in the ND group than in the LPD group. Higher oxidative stress and cytokine levels (TNF-α and IL-6), increased PCNA expression, and pronounced histological alterations were observed in ND mice. PK analysis showed greater C
conclusionOur findings highlight the paradoxical vulnerability of the ND group to AILI and death. Therefore, PMN could be the reason for fewer APAP overdose-related deaths in developing countries. Further, unravelling the precise molecular mechanisms induced by nutritional changes is critical for understanding the paradoxical decline in liver injury associated with PMN.
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