Department of Biosciences, Institute of Health and Society, Federal University of Sao Paulo UNIFESP, Santos SP, Brazil.
Department of Physiology, Universidade São Judas Tadeu, Campus Unimonte, Santos, SP, Brazil.
Int J Environ Health Res. 2022 Sep;32(9):2017-2026. doi: 10.1080/09603123.2021.1934420. Epub 2021 Jun 25.
The aim of this study was to investigate histopathological and inflammatory response in liver and kidney of rats after crack exposure. For this purpose, a total of 32 male Wistar rats were distributed into four groups: (G1) and (G2): received 18 mg/kg of body weight (b.w) of crack cocaine, but Group G2 remained 72 h without exposure after the experimental period (5 days). Experimental group 3 (G3): received 36 mg/kg of body weight (b.w) of crack cocaine. Control Group (CTRL): received only the vehicle (DMSO) administered by intraperitoneal (i.p) route for 5 days. The results showed that crack cocaine induced histopathological changes in liver and kidney. Immunohistochemistry data revealed that G2 group showed a higher immunoexpression of Ki-67 in hepatic and renal tissues. Regarding inflammation, the results showed that all groups exposed to crack cocaine decreased the expression of TNF-α, IL-6, and IL-10 in liver and kidney. In summary, our results showed that the subacute doses of crack cocaine used in this study had cytotoxic, and immunosuppressive effects in liver and kidney of rats, especially at 36 mg/kg dose. Since cellular death and inflammation participates in the multi-step process of chemical carcinogenesis, these data offer new insights into potential ways to understand the pathobiological mechanisms induced by crack cocaine in several tissues and organs.
本研究旨在探讨可卡因暴露后大鼠肝、肾的组织病理学和炎症反应。为此，将 32 只雄性 Wistar 大鼠随机分为四组：（G1）和（G2）：分别给予 18mg/kg 体重的可卡因，但 G2 组在实验期（5 天）后 72h 无暴露。实验组 3（G3）：给予 36mg/kg 体重的可卡因。对照组（CTRL）：仅通过腹腔内（i.p）途径给予 DMSO 载体，连续 5 天。结果表明，可卡因诱导了肝、肾的组织病理学变化。免疫组织化学数据显示，G2 组肝、肾组织中 Ki-67 的免疫表达更高。关于炎症，结果表明，所有暴露于可卡因的组均降低了肝、肾组织中 TNF-α、IL-6 和 IL-10 的表达。总之，本研究中使用的亚急性可卡因剂量对大鼠的肝、肾具有细胞毒性和免疫抑制作用，尤其是在 36mg/kg 剂量下。由于细胞死亡和炎症参与了化学致癌的多步骤过程，这些数据为理解可卡因在多个组织和器官中诱导的病理生物学机制提供了新的见解。
