To delineate the cellular and molecular mechanisms underlying cocaine-induced cytotoxicity, emphasizing the significance of sigma-1 receptors and adulterants in public health.
Key Findings:
Cocaine induces significant cytotoxic effects across multiple biological systems, particularly in the CNS, cardiovascular, hepatic, and renal tissues.
Oxidative stress and redox imbalance are central to cocaine's cytotoxic effects, leading to neuronal death and DNA damage.
Adulterants like phenacetin, levamisole, and caffeine exacerbate cocaine's cytotoxicity through synergistic interactions.
Sigma-1 receptors critically modulate the cellular environment and mediate cocaine's toxic effects.
Interpretation:
Cocaine's cytotoxicity is multifaceted, involving direct neurotoxic effects and exacerbation by adulterants, with sigma-1 receptors serving as a key mediator, highlighting implications for treatment strategies.
Limitations:
The review primarily focuses on in vitro and in vivo models, which may not fully replicate human responses, and potential biases in the studies reviewed.
Limited exploration of the long-term effects of cocaine and adulterants on different biological systems.
Conclusion:
Cocaine's cytotoxicity is a complex interplay of neurochemical imbalances, oxidative stress, and the influence of adulterants, highlighting the need for further research on sigma-1 receptor modulation and specific areas for future investigation.
by Aline Steinmetz, Carlo Frederico Moro, Luana Freese, Murilo Sander de Abreu, Rodrigo Ligabue Braum, Helena Maria Tannhauser Barros, Dinara Jaqueline Moura
A large audit of biomedical publications suggests fabricated references are increasingly appearing in peer-reviewed papers — often in ways that are difficult for reviewers and readers to detect.
