We investigated the ability of tannic acid (TA) to prevent oxidative and nitrosative damage in the brain, liver, kidney, and serum of a rat model of acute hypermethioninemia. Young Wistar rats were divided into four groups: I (control), II (TA 30 mg/kg), III (methionine (Met) 0.4 g/kg + methionine sulfoxide (MetO) 0.1 g/kg), and IV (TA/Met + MetO). Rats in groups II and IV received TA orally for seven days, and rats of groups I and III received an equal volume of water. After pretreatment with TA, rats from groups II and IV received a single subcutaneous injection of Met + MetO, and were euthanized 3 h afterwards. In specific brain structures and the kidneys, we observed that Met + MetO led to increased reactive oxygen species (ROS), nitrite, and lipid peroxidation levels, followed by a reduction in thiol content and antioxidant enzyme activity. On the other hand, pretreatment with TA prevented both oxidative and nitrosative damage. In the serum, Met + MetO caused a decrease in the activity of antioxidant enzymes, which was again prevented by TA pretreatment. In contrast, in the liver, there was a reduction in ROS levels and an increase in total thiol content, which was accompanied by a reduction in catalase and superoxide dismutase activities in the Met + MetO group, and pretreatment with TA was able to prevent only the reduction in catalase activity. Conclusively, pretreatment with TA has proven effective in preventing oxidative and nitrosative changes caused by the administration of Met + MetO, and may thus represent an adjunctive therapeutic approach for treatment of hypermethioninemia.

我们研究了单宁酸 (TA) 防止急性高甲硫氨酸血症大鼠模型的大脑、肝脏、肾脏和血清中氧化和亚硝化损伤的能力。年轻的 Wistar 大鼠分为四组：I（对照）、II（TA 30 mg/kg）、III（甲硫氨酸（Met）0.4 g/kg + 甲硫氨酸亚砜（MetO）0.1 g/kg）和 IV（TA/ Met + MetO)。II组和IV组大鼠口服TA 7天，I组和III组大鼠接受等体积的水。在用TA预处理后，来自组II和IV的大鼠接受单次皮下注射Met + MetO，并在3小时后安乐死。在特定的大脑结构和肾脏中，我们观察到 Met + MetO 导致活性氧 (ROS)、亚硝酸盐和脂质过氧化水平增加，随后硫醇含量和抗氧化酶活性降低。另一方面，用 TA 预处理可以防止氧化和亚硝化损伤。在血清中，Met + MetO 导致抗氧化酶的活性降低，这再次被 TA 预处理所阻止。相反，在肝脏中，在 Met + MetO 组中，ROS 水平降低，总硫醇含量增加，伴随着过氧化氢酶和超氧化物歧化酶活性的降低，而用 TA 预处理只能预防过氧化氢酶活性降低。总之，TA 预处理已被证明可有效预防由 Met + MetO 给药引起的氧化和亚硝化变化，因此可能代表治疗高甲硫氨酸血症的辅助治疗方法。Met + MetO 导致抗氧化酶活性降低，而 TA 预处理再次阻止了这一点。相反，在肝脏中，在 Met + MetO 组中，ROS 水平降低，总硫醇含量增加，伴随着过氧化氢酶和超氧化物歧化酶活性的降低，而用 TA 预处理只能预防过氧化氢酶活性降低。总之，TA 预处理已被证明可有效预防由 Met + MetO 给药引起的氧化和亚硝化变化，因此可能代表治疗高甲硫氨酸血症的辅助治疗方法。Met + MetO 导致抗氧化酶活性降低，而 TA 预处理再次阻止了这一点。相反，在肝脏中，在 Met + MetO 组中，ROS 水平降低，总硫醇含量增加，伴随着过氧化氢酶和超氧化物歧化酶活性的降低，而用 TA 预处理只能预防过氧化氢酶活性降低。总之，TA 预处理已被证明可有效预防由 Met + MetO 给药引起的氧化和亚硝化变化，因此可能代表治疗高甲硫氨酸血症的辅助治疗方法。ROS 水平降低，总硫醇含量增加，伴随着 Met + MetO 组中过氧化氢酶和超氧化物歧化酶活性的降低，用 TA 预处理只能防止过氧化氢酶活性的降低。总之，TA 预处理已被证明可有效预防由 Met + MetO 给药引起的氧化和亚硝化变化，因此可能代表治疗高甲硫氨酸血症的辅助治疗方法。ROS 水平降低，总硫醇含量增加，伴随着 Met + MetO 组中过氧化氢酶和超氧化物歧化酶活性的降低，用 TA 预处理只能防止过氧化氢酶活性的降低。总之，TA 预处理已被证明可有效预防由 Met + MetO 给药引起的氧化和亚硝基变化，因此可能代表治疗高甲硫氨酸血症的辅助治疗方法。