Онтогенез Drosophila melanogaster як мішень нікотинової токсичності. Повідомлення I
Альтернативна назва
Ontogenesis of Drosophila melanogaster as a target of nicotine toxicity. Part I
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
У роботі досліджено вплив нікобустера для електронних сигарет на розвиток Drosophila melanogaster при пероральному введенні. Показано, що нікотин зумовлює дозозалежну затримку метаморфозу, зниження виживаності та плодючості. Водночас виявлено підвищення ступеня політенізації ядер клітин слинних залоз личинок, що може свідчити про активацію компенсаторних механізмів у відповідь на токсичний стрес. Отримані результати вказують на личинку як критичну мішень дії нікотину та підкреслюють мультифакторний характер його впливу на розвиток D. melanogaster.
Introduction. Despite the well-documented risks, nicotine continues to be widely used globally, both through traditional cigarettes and alternative delivery methods, including among pregnant women. Although many studies have addressed the mechanisms of nicotine’s impact on human health, its effects during early ontogenesis remain poorly understood. While Drosophila melanogaster is extensively used as a model to study nicotine exposure, most research has focused on adult flies: examining behavioral changes, activation of nicotinic acetylcholine receptors (nAChRs), and effects on the dopaminergic system. In contrast, the impact of nicotine on early developmental stages, particularly the larval stage, which is marked by intensive growth, metabolism, and endocrine regulation, has received much less attention. The larval stage, being the main feeding phase of the Drosophila life cycle, may be especially vulnerable to toxicants ingested via the gastrointestinal tract. Although some evidence suggests that nicotine disrupts neuroendocrine coordination of metamorphosis, its effects on larvae remain fragmented. At the cellular level, larval development is accompanied by polytenization, a process influenced by both hormonal balance and environmental factors, including toxicants. However, the role of nicotine in modulating polytenization patterns (potentially a sensitive indicator of stress and metabolic adaptation) has not yet been adequately explored. Therefore, investigating the effects of oral nicotine exposure during Drosophila development is essential for understanding its fundamental mechanisms of action and for extrapolating these findings to other biological systems. Aim. To assess the impact of nicotine derived from a commercial nicotine booster (nicobooster) on Drosophila melanogaster development, including developmental timing, fertility, survival, and the degree of polytenization in salivary gland cells at the larval stage. Methods. Wild-type Drosophila melanogaster (Canton-S strain) were reared on standard culture medium supplemented with a commercial nicotine booster designed for e-cigarettes at concentrations of 0.1, 0.2, and 0.3 mg/mL. A control group was reared on nicotine-free medium. Across experimental and control groups, the following parameters were measured: developmental duration (LT50), reproductive capacity, adult lifespan, and post-embryonic mortality of offspring. Cellular responses to nicotine exposure were analyzed using the model of polytene chromosomes in third-instar larval salivary glands. Nuclear ploidy was assessed based on the frequency distribution of polytenization degrees and the mean polyteny index. Statistical analyses included Student’s t-test, Pearson’s chi-squared test, and Kruskal–Wallis test to determine significant differences among treatment groups. Results. Nicotine from e-cigarette liquids caused a dose-dependent delay in Drosophila melanogaster ontogenesis, evident across all developmental stages, from embryo to imago. At the lowest concentration (0.1 mg/mL), a delay in metamorphosis was observed, while higher concentrations (0.2 and 0.3 mg/mL) led to a significant reduction in the number of pupae, increased time to pupation, and decreased larval survival. The total number of adult flies was reduced 4–5-fold, with post-embryonic mortality reaching up to 40%, indicating substantial toxicity of nicotine for pre-imaginal stages. Interestingly, despite overall suppression of vital functions, an increase in the degree of polytenization was observed in the salivary gland cells of larvae reared on nicotine-containing medium. The highest polyteny levels occurred at 0.2 mg/mL, accompanied by an increased proportion of nuclei undergoing 9–10 endoreduplication cycles. This response may reflect the activation of compensatory cellular mechanisms under toxic stress, potentially mediated by endocrine regulators such as juvenile hormone and ecdysone. Conclusions. Oral exposure to nicotine boosters induces a dose-dependent developmental delay, reduced fertility, and increased post-embryonic mortality in D. melanogaster. Nicotine triggers compensatory mechanisms such as enhanced polytenization, increasing genomic copy number in salivary gland cells, which may represent an adaptive response to toxic stress.
Introduction. Despite the well-documented risks, nicotine continues to be widely used globally, both through traditional cigarettes and alternative delivery methods, including among pregnant women. Although many studies have addressed the mechanisms of nicotine’s impact on human health, its effects during early ontogenesis remain poorly understood. While Drosophila melanogaster is extensively used as a model to study nicotine exposure, most research has focused on adult flies: examining behavioral changes, activation of nicotinic acetylcholine receptors (nAChRs), and effects on the dopaminergic system. In contrast, the impact of nicotine on early developmental stages, particularly the larval stage, which is marked by intensive growth, metabolism, and endocrine regulation, has received much less attention. The larval stage, being the main feeding phase of the Drosophila life cycle, may be especially vulnerable to toxicants ingested via the gastrointestinal tract. Although some evidence suggests that nicotine disrupts neuroendocrine coordination of metamorphosis, its effects on larvae remain fragmented. At the cellular level, larval development is accompanied by polytenization, a process influenced by both hormonal balance and environmental factors, including toxicants. However, the role of nicotine in modulating polytenization patterns (potentially a sensitive indicator of stress and metabolic adaptation) has not yet been adequately explored. Therefore, investigating the effects of oral nicotine exposure during Drosophila development is essential for understanding its fundamental mechanisms of action and for extrapolating these findings to other biological systems. Aim. To assess the impact of nicotine derived from a commercial nicotine booster (nicobooster) on Drosophila melanogaster development, including developmental timing, fertility, survival, and the degree of polytenization in salivary gland cells at the larval stage. Methods. Wild-type Drosophila melanogaster (Canton-S strain) were reared on standard culture medium supplemented with a commercial nicotine booster designed for e-cigarettes at concentrations of 0.1, 0.2, and 0.3 mg/mL. A control group was reared on nicotine-free medium. Across experimental and control groups, the following parameters were measured: developmental duration (LT50), reproductive capacity, adult lifespan, and post-embryonic mortality of offspring. Cellular responses to nicotine exposure were analyzed using the model of polytene chromosomes in third-instar larval salivary glands. Nuclear ploidy was assessed based on the frequency distribution of polytenization degrees and the mean polyteny index. Statistical analyses included Student’s t-test, Pearson’s chi-squared test, and Kruskal–Wallis test to determine significant differences among treatment groups. Results. Nicotine from e-cigarette liquids caused a dose-dependent delay in Drosophila melanogaster ontogenesis, evident across all developmental stages, from embryo to imago. At the lowest concentration (0.1 mg/mL), a delay in metamorphosis was observed, while higher concentrations (0.2 and 0.3 mg/mL) led to a significant reduction in the number of pupae, increased time to pupation, and decreased larval survival. The total number of adult flies was reduced 4–5-fold, with post-embryonic mortality reaching up to 40%, indicating substantial toxicity of nicotine for pre-imaginal stages. Interestingly, despite overall suppression of vital functions, an increase in the degree of polytenization was observed in the salivary gland cells of larvae reared on nicotine-containing medium. The highest polyteny levels occurred at 0.2 mg/mL, accompanied by an increased proportion of nuclei undergoing 9–10 endoreduplication cycles. This response may reflect the activation of compensatory cellular mechanisms under toxic stress, potentially mediated by endocrine regulators such as juvenile hormone and ecdysone. Conclusions. Oral exposure to nicotine boosters induces a dose-dependent developmental delay, reduced fertility, and increased post-embryonic mortality in D. melanogaster. Nicotine triggers compensatory mechanisms such as enhanced polytenization, increasing genomic copy number in salivary gland cells, which may represent an adaptive response to toxic stress.
Опис
Ключові слова
Drosophila melanogaster, нікобустер, нікотин, розвиток, політенні хромосоми, плодючість, фітнес, токсичний стрес, nicobooster, nicotine, development, polytene chromosomes, fertility, fitness, toxic stress
Бібліографічний опис
Білоконь С. В. Онтогенез Drosophila melanogaster як мішень нікотинової токсичності. Повідомлення I / С. В. Білоконь, Т. Г. Алєксєєва, В. О. Сачалко // Вісник Одеського національного університету. Біологія. – 2025. – Т. 30, вип. 1(56). – С. 43–70.
УДК
595.773.4:591.3