Indian journal of pharmacology · 2026
Modulation of mineralocorticoid receptor protects tributyltin chloride-induced early neurotoxic anomalies in rats.
СтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Singh Kamendra, Tyagi Sachin, Aggarwal Himanshu
Аннотация
BACKGROUND: Tributyltin chloride (TBTC) is an organotin (OT) compound, a known neurotoxin and an endocrine disruptor, but it is inadequately characterized for its short-term exposure. This study aimed to explore the role of N-acetylcysteine (NAC) and Eplerenone in TBTC induced neurotoxicity in rats.
MATERIALS AND METHODS: Rats were exposed to a single dose of TBTC and were behaviorally assessed on open field test, light and dark box, Morris water maze, and rota rod test. Thiobarbituric acid reactive substances (TBARS) and nitrite were estimated as a measure of oxidative and nitrosative stress. Evans blue extravasation was used to assess the blood-brain barrier (BBB) integrity and morphological changes were assessed by histopathology. NAC (50 mg/kg) was used as a standard treatment, and eplerenone (50 and 100 mg/kg) was used as test interventions.
RESULTS: Short-term TBTC exposure produced significant anxiety-like behavioral alterations, accompanied by elevated brain TBARS and serum nitrite levels, indicating enhanced oxidative and nitrosative stress. BBB integrity was disrupted, and histopathological examination revealed early structural changes. Treatment with NAC and Eplerenone significantly attenuated behavioral disturbances, oxidative stress markers, BBB disruption, and histopathological damage. In contrast, no significant deficits were observed in spatial memory or motor coordination, likely due to the limited exposure duration.
CONCLUSION: TBTC induced early neurotoxic changes in the brain, which were attenuated by NAC and eplerenone administration. The beneficial effects support for further mechanistic studies on mineralocorticoid receptor modulation as a potential target for OT-induced neurotoxicity.
MATERIALS AND METHODS: Rats were exposed to a single dose of TBTC and were behaviorally assessed on open field test, light and dark box, Morris water maze, and rota rod test. Thiobarbituric acid reactive substances (TBARS) and nitrite were estimated as a measure of oxidative and nitrosative stress. Evans blue extravasation was used to assess the blood-brain barrier (BBB) integrity and morphological changes were assessed by histopathology. NAC (50 mg/kg) was used as a standard treatment, and eplerenone (50 and 100 mg/kg) was used as test interventions.
RESULTS: Short-term TBTC exposure produced significant anxiety-like behavioral alterations, accompanied by elevated brain TBARS and serum nitrite levels, indicating enhanced oxidative and nitrosative stress. BBB integrity was disrupted, and histopathological examination revealed early structural changes. Treatment with NAC and Eplerenone significantly attenuated behavioral disturbances, oxidative stress markers, BBB disruption, and histopathological damage. In contrast, no significant deficits were observed in spatial memory or motor coordination, likely due to the limited exposure duration.
CONCLUSION: TBTC induced early neurotoxic changes in the brain, which were attenuated by NAC and eplerenone administration. The beneficial effects support for further mechanistic studies on mineralocorticoid receptor modulation as a potential target for OT-induced neurotoxicity.