Оцінка маркерів окисного стресу та клітинного ушкодження в органах щурів за дії електронних сигарет
Альтернативна назва
Assessment of oxidative stress markers and cellular damage in rat organs under the influence of electronic cigarettes
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Файли
Дата
2025
Науковий керівник
Укладач
Редактор
Назва журналу
ISSN
2077-1746
E-ISSN
2415-3125
Назва тому
Видавець
Одеський національний університет імені І. І. Мечникова
Анотація
Досліджено вплив парів електронних сигарет на показники оксидативного стресу та функціональний стан тканин щурів Wistar за тримісячної пасивної інгаляційної експозиції. Виявлено достовірне підвищення окисної модифікації білків та рівня малонового діальдегіду у легенях, печінці, серцевому м’язі, нирках та мозку, що свідчить про системний оксидативний стрес. Зміни активності ферментів ГГТ, АЛТ, АСТ та ЛФ відображають метаболічну перебудову та структурно-функціональні ушкодження органів, підкреслюючи потенційні токсикологічні ризики інгаляційного впливу компонентів електронних сигарет.
Problem. Electronic cigarettes have become increasingly popular among Ukrainian youth, with 19,6% of adolescents aged 13–15 and approximately 45% of young adults aged 18–29 using them. Studies indicate that e-cigarette liquids exhibit cytotoxic effects and generate toxic carbonyl compounds (formaldehyde, acetaldehyde, acrolein) and reactive oxygen species upon heating. Contact with metal heating elements also releases heavy metal ions (nickel, chromium, cadmium, lead), inducing oxidative damage to proteins, lipids, and DNA. Experimental rat models allow assessment of biochemical, morphological, and metabolic disturbances at the organ level, confirming the risk of systemic oxidative stress and tissue injury. Aim. The study aimed to evaluate biochemical changes in rat tissues (heart, brain, kidneys, lungs, and liver) under exposure to e-cigarette aerosol through a comprehensive analysis of protein oxidative modification (OMP) products, lipid peroxidation measured by malondialdehyde (MDA) levels, and the activity of cytolysis marker enzymes — γ-glutamyltransferase (GGT), alkaline phosphatase (ALP), aspartate aminotransferase (AST), and alanine aminotransferase (ALT). Methods. A passive smoking model was implemented using 20 adult male Wistar rats (8–10 weeks old, 180–220 g), divided into experimental (n = 10) and control (n = 10) groups. Rats in the experimental group were exposed daily for 20 minutes to aerosol from an Elf Bar 1500 Ultra e-cigarette (China) at a rate of 100 ml/min, while control rats were not exposed. After three months, animals were euthanized in accordance with standard ethical protocols, and tissues were collected for analysis. Main results. The highest increases in protein oxidative modification were observed in the lungs and liver, indicating active formation of oxidative products. Malondialdehyde levels were most elevated in the lungs, reflecting lipid peroxidation. In lung tissue, decreased activities of GGT, ALP, ALT, and AST suggest adaptation to chronic toxic exposure. In the heart, increased GGT and ALP activities indicate activation of antioxidant defense and compensatory responses. In the kidneys, GGT activity increased by nearly 50%, reflecting activation of glutathione-mediated antioxidant defense. Elevated ALT and AST activities indicate moderate cytolysis and mitochondrial activation, suggesting metabolic remodeling and systemic oxidative stress. Liver tissue showed decreased GGT, ALP, ALT activities, with increased AST activity, reflecting adaptive-compensatory responses to chronic toxic exposure and possible mitochondrial injury. Conclusions. Inhalation of electronic cigarette aerosol induces systemic oxidative stress accompanied by metabolic and structural organ remodeling. This is confirmed by experimental data showing significant increases in protein oxidative modification products in the liver, lungs, and heart. Malondialdehyde levels rose in all studied organs, indicating activation of lipid peroxidation. Increased GGT activity reflects activation of antioxidant defense, while changes in ALT and AST indicate adaptive responses and cytolysis status. Alkaline phosphatase exhibited organ-specific responses, suggesting impaired membrane stability and reduced reparative capacity of cells.
Problem. Electronic cigarettes have become increasingly popular among Ukrainian youth, with 19,6% of adolescents aged 13–15 and approximately 45% of young adults aged 18–29 using them. Studies indicate that e-cigarette liquids exhibit cytotoxic effects and generate toxic carbonyl compounds (formaldehyde, acetaldehyde, acrolein) and reactive oxygen species upon heating. Contact with metal heating elements also releases heavy metal ions (nickel, chromium, cadmium, lead), inducing oxidative damage to proteins, lipids, and DNA. Experimental rat models allow assessment of biochemical, morphological, and metabolic disturbances at the organ level, confirming the risk of systemic oxidative stress and tissue injury. Aim. The study aimed to evaluate biochemical changes in rat tissues (heart, brain, kidneys, lungs, and liver) under exposure to e-cigarette aerosol through a comprehensive analysis of protein oxidative modification (OMP) products, lipid peroxidation measured by malondialdehyde (MDA) levels, and the activity of cytolysis marker enzymes — γ-glutamyltransferase (GGT), alkaline phosphatase (ALP), aspartate aminotransferase (AST), and alanine aminotransferase (ALT). Methods. A passive smoking model was implemented using 20 adult male Wistar rats (8–10 weeks old, 180–220 g), divided into experimental (n = 10) and control (n = 10) groups. Rats in the experimental group were exposed daily for 20 minutes to aerosol from an Elf Bar 1500 Ultra e-cigarette (China) at a rate of 100 ml/min, while control rats were not exposed. After three months, animals were euthanized in accordance with standard ethical protocols, and tissues were collected for analysis. Main results. The highest increases in protein oxidative modification were observed in the lungs and liver, indicating active formation of oxidative products. Malondialdehyde levels were most elevated in the lungs, reflecting lipid peroxidation. In lung tissue, decreased activities of GGT, ALP, ALT, and AST suggest adaptation to chronic toxic exposure. In the heart, increased GGT and ALP activities indicate activation of antioxidant defense and compensatory responses. In the kidneys, GGT activity increased by nearly 50%, reflecting activation of glutathione-mediated antioxidant defense. Elevated ALT and AST activities indicate moderate cytolysis and mitochondrial activation, suggesting metabolic remodeling and systemic oxidative stress. Liver tissue showed decreased GGT, ALP, ALT activities, with increased AST activity, reflecting adaptive-compensatory responses to chronic toxic exposure and possible mitochondrial injury. Conclusions. Inhalation of electronic cigarette aerosol induces systemic oxidative stress accompanied by metabolic and structural organ remodeling. This is confirmed by experimental data showing significant increases in protein oxidative modification products in the liver, lungs, and heart. Malondialdehyde levels rose in all studied organs, indicating activation of lipid peroxidation. Increased GGT activity reflects activation of antioxidant defense, while changes in ALT and AST indicate adaptive responses and cytolysis status. Alkaline phosphatase exhibited organ-specific responses, suggesting impaired membrane stability and reduced reparative capacity of cells.
Опис
Ключові слова
електронні сигарети, біохімічні маркери, токсичність, органоспецифічність, оксидативний стрес, electronic cigarettes, biochemical markers, toxicity, organ specificity, oxidative stress
Бібліографічний опис
Грідіна І. Р., Чернадчук С. С. Оцінка маркерів окисного стресу та клітинного ушкодження в органах щурів за дії електронних сигарет. Вісник Одеського національного університету. Біологія. 2025. Т. 30, вип. 2(57). С. 9–24.
УДК
577.152:615.9:599.323