Mephedrone and Nicotine: Oxidative Stress and Behavioral Interactions in Animal Models

Abstract

The purpose of our experiment was to examine the influence of co-administration of nicotine and mephedrone on anxiety-like behaviors, cognitive processes and the nicotine-induced behavioral sensitization as well as processes connected with induction of oxidative stress in the brain of male Swiss mice. The results revealed that co-administration of subthreshold doses of mephedrone and nicotine (0.05 mg/kg each) exerted marked anxiogenic profile in the elevated plus maze and displayed pro-cognitive action in the passive avoidance paradigm (nicotine 0.05 mg/kg and mephedrone 2.5 mg/kg). Furthermore, one of the main findings of the present study was that mephedrone, administered alone at the dose not affecting locomotor activity of mice (1 mg/kg), enhanced the expression of nicotine-induced locomotor sensitization. Moreover, mephedrone administered with nicotine decreased general antioxidant status and catalase activity as well as antioxidant enzymes activity in the hippocampus and prefrontal cortex and increased concentration of malondialdehyde, an indicator of lipid peroxidation processes. Considering the likelihood that mephedrone is taken as a part of polydrug combination with nicotine, the effects of this combination on mammalian organisms have been confirmed in our study. Understanding the consequences of co-administration of psychoactive substances on the central nervous system and oxidative processes in the brain provide the important toxicological significance, and may be useful in polydrug intoxication treatment. Electronic supplementary materialThe online version of this article (doi:10.1007/s11064-015-1566-5) contains supplementary material, which is available to authorized users.

The Effects of Exposure to Mephedrone During Adolescence on Brain Neurotransmission and Neurotoxicity in Adult Rats

“…These data are in accordance with our findings as we observed oxidative damage of DNA in cortical cells in this region. The induction of oxidative stress evidenced by decreased total antioxidant status, increase in malondialdehyde concentration, and increase in catalase activity was also found in the mouse frontal cortex (Budzynska et al 2015 ). These data confirm our findings on possible oxidative injury of subpopulation of cortical cells.…”

Correlations between the Memory-Related Behavior and the Level of Oxidative Stress Biomarkers in the Mice Brain, Provoked by an Acute Administration of CB Receptor Ligands

“…However, in our experiments we observed that AM 251, a CB1 receptor antagonist, improved cognitive-related processes assessed in the PA test and caused the increase in concentration of MDA. Additionally, we have also performed studies on mephedrone, a synthetic club drug, that induced oxidative stress within brain and its structures responsible for the cognitive functions and also facilitated acquisition and consolidation of the memory processes at the same time [ 76 ]. Similar relationship was observed in the study dealing with nicotine, a nicotinic receptor agonist, which is also prooxidative drug that improves memory functions [ 34 , 76 ].…”

The effect of green tea consumption on the expression of antioxidant‐ and inflammation‐related genes induced by nicotine

“…Nicotine is a naturally occurring alkaloid found in the tobacco plant ( Nicotiana tabacum ) (Moghbel, Ryu, Ratsch, & Steadman, ). It induces oxidative stress both in vitro and in vivo (Budzynska, Boguszewska‐Czubara, Kruk‐Slomka, Kurzepa, & Biala, ). Moreover, nicotine exposure increases free radicals production (mediators of inflammation) and cooperative lipid peroxidation levels in various tissues (Ben Saad et al, ).…”