Nitrate pollution has emerged as a problem of great importance because in recent years, the levels of nitrate in soil and groundwater have increased, mainly through anthropogenic activities, such as the use of fertilizers in agriculture, domestic wastewater and septic tanks, industrial waste and deforestation. In animals, nitrate reduction to nitrite (NO₂) and nitric oxide (NO) promote the formation of methemoglobin in the blood and the generation of highly reactive intermediates that induce oxidative stress in target organs. Exposition to nitrates has been associated with methemoglobinemia, reproductive toxicity, metabolic and endocrine alterations and cancer. This study analyzed acute intoxication with sodium nitrate (NaNO₃) in male Wistar rats, aged 12–16 weeks. Four groups with n = 10 rats each were formed: group 1 was the control, and group 2, group 3 and group 4 were treated for 10 days with intragastric doses of 19, 66 and 150 mg/kg/d NaNO₃, respectively. Hematological, metabolic and histological biomarkers in the liver were analyzed. The results showed high percentages of methemoglobin, an increase in NO₂ in the plasma and an accumulation in the liver. Moreover, there were high counts of white blood cells and platelets in all treated groups. Additionally, there was an increase in the spleen weight in group 4. High levels of glucose, triglycerides, lactate dehydrogenase (LDH), alanine aminotransferase (ALT), and aspartate aminotransferase (AST) were observed and were significantly increased in groups 3 and 4. For oxidative stress biomarkers, there were increases in Thiobarbituric Acid Reactive Substances (TBARS), total GSH and SOD activity, mainly in group 4. Changes in mitochondrial activity were not significant. Histopathological analyses of the liver showed inflammation, infiltration of mononuclear cells, steatosis, ischemia and necrosis, and these findings were more evident at high doses of NaNO₃ in which high of S-nitrosylation were found. In conclusion, NaNO₃ was reduced to NO₂, thereby inducing methemoglobinemia, whereas other reactive species generated oxidative stress, causing hematological and metabolic alterations and injury to the liver.

硝酸盐污染已成为一个非常重要的问题，因为近年来，土壤和地下水中硝酸盐的含量增加了，主要是通过人为活动，例如在农业中使用化肥，生活废水和化粪池，工业废物和森林砍伐。在动物体内，硝酸盐还原为亚硝酸盐（NO ₂）和一氧化氮（NO）会促进血液中高铁血红蛋白的形成，并促进在靶器官中引起氧化应激的高反应性中间体的产生。暴露于硝酸盐与高铁血红蛋白血症，生殖毒性，代谢和内分泌改变以及癌症有关。这项研究分析了硝酸钠（NaNO ₃）在12-16周龄的雄性Wistar大鼠中。形成四组，每组n = 10只大鼠：第1组为对照组，第2组，第3组和第4组分别以19、66和150 mg / kg / d NaNO _3的胃内剂量治疗10天。分析了肝脏中的血液，代谢和组织学生物标志物。结果显示高铁血红蛋白百分比，NO ₂增加在血浆中和肝脏中的积累。此外，在所有治疗组中都有大量白细胞和血小板。此外，第4组的脾脏重量增加。在第3组和第4组中观察到高水平的葡萄糖，甘油三酸酯，乳酸脱氢酶（LDH），丙氨酸氨基转移酶（ALT）和天冬氨酸氨基转移酶（AST）。对于氧化应激生物标志物，主要在组4中，硫代巴比妥酸反应性物质（TBARS），总GSH和SOD活性有所增加。肝脏的组织病理学分析显示炎症，单核细胞浸润，脂肪变性，局部缺血和坏死，这些发现在高剂量的NaNO _3时更明显其中发现高的S-亚硝基化。总之，NaNO ₃还原为NO ₂，从而引起高铁血红蛋白血症，而其他反应性物种产生氧化应激，从而引起血液和代谢改变以及对肝脏的伤害。