Cytotoxicity associated with acute and chronic administration of synthetic cannabinoids “Strox” in the brain, liver, heart, and testes of male albino rats: histological and immunohistochemical study

Abstract

BackgroundSynthetic cannabinoids are one of the largest groups of new psychoactive substances that invaded Egypt’s drug abuse market over the past few years.AimRandomized controlled trial study to demonstrate the effects of acute and chronic toxicity by synthetic cannabinoid (Strox) on the brain, liver, heart, and testes in adult male albino rats through histopathological examination by light microscope and immunohistochemistry.MethodsTotal number of fifty male albino rats were divided into five different groups, two control and three treated groups. Negative and positive control groups received distilled water and dimethyl sulfoxide, respectively, acute group received LD50 (lethal dose 50) once and observed for 14 days, chronic group received 1/10 LD50 for 3 months, and finally chronic withdrawal groups received 1/10 LD50 for 3 months and then left 2 weeks without the substance to observe the withdrawal manifestations.ResultsThe current study revealed various histopathological changes in all organs with increased expression of cannabinoid receptor 1. The most important findings observed by light microscope examination were shrinkage and degenerative changes in Purkinje cells in brain sections, abnormalities in blood sinusoids and architecture in liver section, disruption in cardiac muscle fiber in heart sections, and finally testes showed irregularities in seminiferous tubules and germinal cells. Immunohistochemical staining for caspase-3 in the brain, liver, and heart showed weak-positive reaction in acute group and a strong reaction with chronic groups. Additionally, increase in collagen fiber was observed in sections of the liver and heart of chronic group.ConclusionsSynthetic cannabinoid sample (Strox) toxicity caused adverse effects on the brain, liver, heart, and testes as shown by increasing cannabinoid receptor 1 and caspase-3 expression.