娱乐性MDMA剂量在正常和高温下不会引起HepG2球体的肝毒性
Arthur L de Oliveira1, Raul G Miranda2, Daniel J Dorta1
1Department of Chemistry, Faculty of Philosophy, Sciences and Letters at Ribeirão Preto, University of São Paulo, Ribeirão Preto, SP 14040-901, Brazil.
Toxicology
|February 24, 2024
概括
3,4-甲基二氧化甲胺 (MDMA) 的娱乐剂量在实验室测试中没有导致肝损伤,即使增加了热量. 这表明,MDMA在治疗和降低危害方面可能比以前想象的更安全.
科学领域:
- 药理学 药理学是指药理学的学科.
- 肝毒性 肝毒性 肝毒性
- 神经科学是一个神经科学.
背景情况:
- 3,4-甲基二氧化甲胺 (MDMA) 以其同情效应和在娱乐场所的使用而闻名.
- 高剂量的MDMA与肝损伤和高热症有关,但娱乐用剂量对肝毒性的影响尚不清楚.
- MDMA对恐惧灭绝和记忆再巩固的影响表明,在PTSD等神经精神障碍中可能有治疗应用.
研究的目的:
- 用3D细胞培养模型评估MDMA在娱乐剂量的肝毒性.
- 为了研究正常热与高热对MDMA诱导的肝损伤的影响.
- 评估MDMA在潜在治疗和减少危害方面的安全性.
主要方法:
- 使用HepG2球体作为3D细胞培养模型进行毒性评估.
- 在正常热和高热条件下以娱乐剂量服用MDMA.
- 使用MTT减少试验评估细胞活力,并评估细胞应激的标记物,包括活性氧物种,线粒体膜潜力,细胞循环停止和细胞亡.
主要成果:
- 娱乐用剂量的MDMA并没有显著降低HepG2球体的细胞活力.
- 没有观察到活性氧物种生产的显著增加.
- 即使在高温条件下,MDMA也没有诱导线粒体功能障碍,细胞循环停止或细胞死亡,甚至在高温条件下也没有.
结论:
- 在娱乐用剂量的MDMA似乎不会在HepG2球状模型中引起显著的肝毒性.
- 这些发现支持进一步临床前研究MDMA在降低危害和治疗应用中的安全性的可能性.
- 娱乐用剂量和治疗用剂量之间的重叠要求继续研究MDMA的安全性.
相关概念视频
Increased Body Temperature
6.4K
A body temperature above 38°C (100.4 °F) is known as fever or pyrexia, and a person with fever is termed 'febrile.' Typically, the hypothalamus, a part of the brain that acts as the body's thermostat, regulates body temperature through a thermoregulatory setpoint. It receives signals from cold and warm thermal receptors throughout the body and adjusts the body's temperature accordingly. Fever occurs when this hypothalamic setpoint is altered, usually in...
6.4K
Homeostatic Imbalances in Body Temperature
3.9K
Hyperthermia occurs when the body's temperature becomes unusually high, often due to heat exposure, intense physical activity, or certain illnesses. This condition can create a dangerous cycle where elevated body temperature increases the metabolic rate, generating more heat and potentially leading to organ failure and brain damage. A severe form of hyperthermia, called heat stroke, can raise body temperature to life-threatening levels. Fever, on the other hand, is a controlled form of...
3.9K
Effect of Hepatic Disease on Pharmacokinetics: Pathophysiologic Assessment and Liver Function Test
271
In clinical practice, the direct measurement of hepatic blood flow to evaluate liver function presents significant challenges due to the intricate and specialized nature of the necessary techniques. Consequently, healthcare professionals often rely on empirical estimates derived from thorough patient examinations and liver function tests to gauge liver health. Among the tools at their disposal, the Child–Pugh and MELD scoring systems stand out for their ability to categorize and assess...
271
Effect of Hepatic Disease on Pharmacokinetics: Dose Adjustments Due to Hepatic Impairment
379
Hepatic impairment, characterized by decreased liver function, does not uniformly mandate adjustments in drug dosage. Whether dosage modifications are necessary depends on various factors related to the drug's metabolism and elimination pathways. If a drug is primarily excreted via the kidneys and bypasses significant hepatic processing, if it undergoes minimal metabolic transformation in the liver, or if it is volatile and primarily expelled through the lungs, dose adjustments may not be...
379
Drug Toxicity: Dose-Dependent Reactions
229
Drug toxicities can be stratified into pharmacological, pathological, or genotoxic based on their mechanisms. The incidence and severity of these toxicities generally increase with the drug's concentration in the body and exposure time.Pharmacological toxicity is evident when the therapeutic effects of drugs overshoot into adverse reactions in a predictable, dose-dependent manner. Central nervous system (CNS) depression from barbiturates is a classic example, with effects escalating from...
229
Hepatitis
86
Hepatitis is an inflammatory condition of the liver most commonly caused by hepatotropic viruses (A–E), though non-infectious causes such as alcohol and drugs also exist.Hepatitis AHepatitis A virus (HAV) is a non-enveloped RNA virus of the Picornaviridae family. It is primarily transmitted via the fecal-oral route, typically through ingestion of contaminated food or water. After ingestion, HAV enters the bloodstream through the oropharynx or intestinal epithelium and reaches the liver.
86


