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Abstract：
BACKGROUND: The study determined the damage caused by formaldehyde (FA) exposure in blood and liver samples using biochemical markers. Histopathological analysis was performed using the terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) method and measurement of CD68 cell density. To what extent the antioxidant molecules thymoquinone (TQ) and ozone (O3) reversed the damage caused by FA exposure was investigated, both when used alone and combined.
METHODS: Fifty-six Sprague-Dawley male rats of eight to ten weeks of age were used in the experiment. The rats were divided into eight groups, with seven rats in each group: the untreated control group, the group treated with TQ (10 mg/kg/day), the group treated with O3 (150 μg/kg/day), the group treated with TQ+O3, the group exposed to FA (10 ppm 8 h/day), the group receiving FA+TQ, the group receiving FA+O3, and the group receiving FA+TQ+O3. Serum aspartate transaminase (AST), alanine transaminase (ALT), total antioxidant (TAS, U/mL), and total oxidant (TOS, nmol/mL) levels were analyzed. TAS and TOS levels, CD68 cell density, and apoptotic cells were determined in liver tissues.
RESULTS: FA exposure caused an increase in serum AST and ALT levels of (p<0.05) experimental animals, a decrease in TAS levels in serum (p=0.03) and liver (p>0.05) and an increase in TOS levels (p>0.05), TUNEL positivity (p<0.001), and CD68 cell density (p=0.004). Administration of TQ and O3 as antioxidants significantly reversed biochemical and histopathological alterations in the serum and liver.
CONCLUSIONS: TQ and ozone therapy suppressed oxidative stress caused by FA exposure and reversed the emerging histopathological deteriorations. Ozone therapy did not suppress the effects of TQ. Therefore, ozone therapy can be given as a supportive therapy along with the main therapeutic agents. We think TQ and ozone therapy may be useful to protect individuals exposed to FA.
METHODS: Fifty-six Sprague-Dawley male rats of eight to ten weeks of age were used in the experiment. The rats were divided into eight groups, with seven rats in each group: the untreated control group, the group treated with TQ (10 mg/kg/day), the group treated with O3 (150 μg/kg/day), the group treated with TQ+O3, the group exposed to FA (10 ppm 8 h/day), the group receiving FA+TQ, the group receiving FA+O3, and the group receiving FA+TQ+O3. Serum aspartate transaminase (AST), alanine transaminase (ALT), total antioxidant (TAS, U/mL), and total oxidant (TOS, nmol/mL) levels were analyzed. TAS and TOS levels, CD68 cell density, and apoptotic cells were determined in liver tissues.
RESULTS: FA exposure caused an increase in serum AST and ALT levels of (p<0.05) experimental animals, a decrease in TAS levels in serum (p=0.03) and liver (p>0.05) and an increase in TOS levels (p>0.05), TUNEL positivity (p<0.001), and CD68 cell density (p=0.004). Administration of TQ and O3 as antioxidants significantly reversed biochemical and histopathological alterations in the serum and liver.
CONCLUSIONS: TQ and ozone therapy suppressed oxidative stress caused by FA exposure and reversed the emerging histopathological deteriorations. Ozone therapy did not suppress the effects of TQ. Therefore, ozone therapy can be given as a supportive therapy along with the main therapeutic agents. We think TQ and ozone therapy may be useful to protect individuals exposed to FA.
摘要：
背景：该研究使用生化标志物确定了血液和肝脏样品中甲醛（FA）暴露引起的损害。使用末端脱氧核苷酸转移酶dUTP缺口末端标记(TUNEL)方法和CD68细胞密度的测量进行组织病理学分析。研究了抗氧化剂分子百里香醌（TQ）和臭氧（O3）在多大程度上逆转了FA暴露造成的损害，无论是单独使用还是组合使用。
方法：实验中使用56只8至10周龄的Sprague-Dawley雄性大鼠。将大鼠分成八组,每组7只大鼠：未治疗的对照组，TQ治疗组（10mg/kg/天），O3治疗组（150μg/kg/天），用TQ+O3处理的组，暴露于FA的组（10ppm8小时/天），接受FA+TQ的组，接受FA+O3的组和接受FA+TQ+O3的组。血清天冬氨酸转氨酶(AST),丙氨酸转氨酶(ALT),总抗氧化剂(TAS，U/mL),和总氧化剂(TOS，nmol/mL)水平进行分析。TAS和TOS级别,CD68细胞密度，并在肝组织中确定凋亡细胞。
结果：FA暴露导致（p<0.05）实验动物的血清AST和ALT水平升高，血清（p=0.03）和肝脏（p>0.05）中TAS水平降低，TOS水平升高（p>0.05），TUNEL阳性（p<0.001），和CD68细胞密度(p=0.004)。施用TQ和O3作为抗氧化剂可显着逆转血清和肝脏的生化和组织病理学改变。
结论：TQ和臭氧治疗抑制了由FA暴露引起的氧化应激，并逆转了新出现的组织病理学恶化。臭氧治疗不能抑制TQ的作用。因此,臭氧疗法可以作为支持疗法与主要治疗剂一起给予。我们认为TQ和臭氧治疗可能有助于保护暴露于FA的个体。
方法：实验中使用56只8至10周龄的Sprague-Dawley雄性大鼠。将大鼠分成八组,每组7只大鼠：未治疗的对照组，TQ治疗组（10mg/kg/天），O3治疗组（150μg/kg/天），用TQ+O3处理的组，暴露于FA的组（10ppm8小时/天），接受FA+TQ的组，接受FA+O3的组和接受FA+TQ+O3的组。血清天冬氨酸转氨酶(AST),丙氨酸转氨酶(ALT),总抗氧化剂(TAS，U/mL),和总氧化剂(TOS，nmol/mL)水平进行分析。TAS和TOS级别,CD68细胞密度，并在肝组织中确定凋亡细胞。
结果：FA暴露导致（p<0.05）实验动物的血清AST和ALT水平升高，血清（p=0.03）和肝脏（p>0.05）中TAS水平降低，TOS水平升高（p>0.05），TUNEL阳性（p<0.001），和CD68细胞密度(p=0.004)。施用TQ和O3作为抗氧化剂可显着逆转血清和肝脏的生化和组织病理学改变。
结论：TQ和臭氧治疗抑制了由FA暴露引起的氧化应激，并逆转了新出现的组织病理学恶化。臭氧治疗不能抑制TQ的作用。因此,臭氧疗法可以作为支持疗法与主要治疗剂一起给予。我们认为TQ和臭氧治疗可能有助于保护暴露于FA的个体。
