Hydroquinone Exposure Induces Organ-Specific Antioxidant Alterations and Histopathological Injury in the Liver, Kidney, Lung, and Spleen of Maternal Mice

Abstract

BACKGROUND: Gestational benzene exposure is associated with oxidative stress and fetal toxicity. However, data regarding the organ specificity of oxidative and histopathological injury in maternal tissues during gestation remains widely unexplored. Therefore, this study was conducted to evaluate oxidative damage and histopathological alterations in the liver, kidney, lung, and spleen following maternal benzene exposure.

METHODS: Eighteen pregnant ICR mice (8-10 weeks, 30-40 g) were randomly divided into three groups (n=6/each): healthy mice as control, mice that was given hydroquinone (HQ) orally at 25 mg/kg (HQ25) and 50 mg/kg (HQ50) on gestational day-12, -14, and -16. On gestational day-18, mice were sacrificed and the liver, kidney, lung, and spleen harvested for analysis. Malondialdehyde (MDA), advanced oxidation protein products (AOPP), glutathione (GSH), and superoxide dismutase (SOD) activity were analyzed by measuring thiobarbituric acid‑reactive substances (TBARS), oxidation of potassium iodide (KI), 5,5′‑dithiobis(2‑nitrobenzoic acid) (DTNB), and nitroblue tetrazolium (NBT), respectively. Histopathological analysis was performed using hematoxylin and eosin (H&E) staining.

RESULTS: No significant changes in oxidative stress markers were observed in the organs of HQ-treated groups compared with control group. However, a significant reduction in GSH levels (p=0.02) was detected in the spleen of HQ50 group, while SOD activity (p=0.01) was significantly reduced in the lungs of both HQ-treated groups compared with the control group. Histopathological examination of the HQ-treated groups revealed hepatocyte necrosis in the liver; altered glomerular size, enlarged Bowman's space, increased cellularity, thickening of Bowman's capsule, and degeneration of the proximal tubular brush border in the kidneys; lymphocyte aggregation and increased cellularity in the spleen; and irregular bronchial walls, inflammatory cell infiltration, enlarged alveoli, and epithelial damage in the lungs.

CONCLUSION: HQ exposure induced organ-specific antioxidant alterations and histopathological injury across maternal organs, suggesting differential maternal organ responses to gestational HQ exposure despite unremarkable oxidative damage.

KEYWORDS: benzene, hydroquinone, maternal toxicity, oxidative stress, histopathology