Avaliação morfométrica de danos e status oxidativo hepáticos em camundongos infectados com Toxoplasma gondii em fase aguda e crônica

Abstract

Toxoplasmosis, caused by the obligate intracellular protozoan Toxoplasma gondii, is a widely distributed zoonosis capable of affecting multiple tissues, including the liver. Accordingly, this study aimed to comprehensively evaluate morphometric, biochemical, and histopathological alterations in the liver of experimentally infected C57BL/6 mice, comparing the acute (7 days) and chronic (21 days) phases of infection. A total of 24 male mice were divided into four groups: acute phase (12 animals) — Acute Control (n = 6) and Acute Infected (n = 6); and chronic phase (12 animals) — Chronic Control (n = 6) and Chronic Infected (n = 6). Infected animals received 10 cysts of the ME49 strain of T. gondii orally via gavage. Body weight, liver weight, and hepatosomatic index (HSI) were measured, and liver samples were collected for glycogen, oxidative stress, histological, and morphometric analyses. Glycogen was assessed for both density and content. Oxidative stress was analyzed by determining the enzymatic activities of superoxide dismutase (SOD), catalase (CAT), and glutathione S-transferase (GST), as well as malondialdehyde (MDA), nitric oxide (NO), and total antioxidant capacity (FRAP). Ion transport function was evaluated by measuring ATPase (Na⁺/K⁺, Mg²⁺, and Ca²⁺) activities. Infection by Toxoplasma gondii induced liver alterations modulated by the infection phase, without affecting body weight, glycogen content, or ATPase activity, indicating preserved hepatic energy metabolism and homeostasis. During the acute phase, a decrease in the hepatosomatic index and liver water content was observed, suggesting loss of functional mass and tissue dehydration, whereas in the chronic phase, these variables increased, reflecting compensatory adaptations, including vascular remodeling and fluid retention. Antioxidant activity was modulated, with increased catalase and GST in the chronic phase, highlighting the adaptive response to oxidative stress. Markers of hepatic damage, such as MDA and NO, remained stable, supporting the maintenance of redox balance. Morphometric analyses showed increased cytoplasmic volume and sinusoidal capillaries, with no nuclear alterations or necrosis, while fibrosis, steatosis, and inflammatory infiltrates were absent, indicating moderate liver injury. Clinically, these findings suggest that infection may cause moderate hepatic dysfunction, with potential risks of elevated transaminases and structural alterations, while antioxidant and adaptive mechanisms are essential to limit tissue damage. These results underscore the complex hepatic response to the parasite and highlight the need for human studies to validate biomarkers and guide therapeutic interventions.