Biomarkers of the Antioxidant Response: A Focus on Liver Carcinogenesis

Sánchez‐Rodríguez, Ricardo; Torres-Mena, Julia Esperanza; Pozo‐Yauner, Luis del; Pérez‐Carreón, Julio Isael

doi:10.1007/978-94-007-7675-3_36

Cited by 1 publication

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“…Oxidative stress is largely regulated by the antioxidant enzyme system, including SOD, CAT, GPx, peroxiredoxin (Prx), and glutathione reductase (GSR), among others. Therefore, the loss of expression of these enzymes could be used as biomarkers of oxidative stress [73]. In this study, a downregulation in the expression of genes encoding oxidative stress-scavenging enzymes such as Sod1 (Figure 3B) and Hmox1 (Figure S2) was evidenced, suggesting disturbances in the antioxidant system due to the overproduction of epoxides and other B[a]P byproducts [30,32].…”

Section: Discussionmentioning

confidence: 54%

Exposure to Benzo(a)pyrene Enhances Acetaminophen-Induced Liver Injury in Mice at Non-Hepatotoxic Doses

Montero-Pérez,

Olivero-Verbel

2024

Sci. Pharm.

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Acetaminophen (APAP) is a widely used analgesic, especially for children. Its primary mechanism involves inhibiting cyclooxygenase enzymes and activating the endocannabinoid and TRPV1 systems. Though its toxicity is low, it can harm the liver in a dose-dependent manner. Low APAP doses can also increase pollutant-induced liver damage. Little is known about interactions between APAP and benzo[a]pyrene (B[a]P). This study aimed to assess if co-exposure to non-hepatotoxic doses of B[a]P and APAP causes liver injury in mice, exploring the underlying mechanisms. Female ICR mice received 50 mg/kg B[a]P or a vehicle for three days, followed by 200 mg/kg APAP or a vehicle. Liver injury was assessed through histopathological examination, serum transaminase activity, and gene expression analysis. In the B[a]P/APAP group, several histology changes were observed, including ballooning injury, steatosis, necrosis, inflammation, and apoptosis. Transaminase levels correlated with histopathological scores, and there was an increase in hepatic cytochrome P450 family 1 subfamily a member 1 (Cyp1a1) mRNA levels and a decrease in aryl hydrocarbon receptor (Ahr), cytochrome P450 family 2 subfamily e polypeptide 1 (Cyp2e1), superoxide dismutase 1 (Sod1), peroxisome proliferator activated receptor gamma (Ppar-γ), and caspase 3 (Casp3). This suggests that prior exposure to B[a]P makes mice more susceptible to APAP-induced liver injury, involving changes in gene expression related to metabolism, redox balance, and cell proliferation. Therefore, using therapeutic APAP doses after exposure to B[a]P could lead to liver injury.

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Section: Discussionmentioning

confidence: 54%