Abstract

Whilst mitochondrial inhibition and micronuclear fragmentation are well established features of the cannabis literature mitochondrial stress and dysfunction has recently been shown to be a powerful and direct driver of micronucleus formation and chromosomal breakage by multiple mechanisms. In turn genotoxic damage can be expected to be expressed as increased rates of cancer, congenital anomalies and aging; pathologies which are increasingly observed in modern continent-wide studies. Whilst cannabinoid genotoxicity has long been essentially overlooked it may in fact be all around us through the rapid induction of aging of eggs, sperm, zygotes, foetus and adult organisms with many lines of evidence demonstrating transgenerational impacts. Indeed this multigenerational dimension of cannabinoid genotoxicity reframes the discussion of cannabis legalization within the absolute imperative to protect the genomic and epigenomic integrity of multiple generations to come.

RAS ID

77398

Document Type

Journal Article

Date of Publication

11-1-2024

Volume

29

Issue

11

PubMed ID

39538372

School

School of Medical and Health Sciences

Creative Commons License

Creative Commons Attribution 4.0 License
This work is licensed under a Creative Commons Attribution 4.0 License.

Publisher

Wiley

Identifier

Albert Stuart Reece: https://orcid.org/0000-0002-3256-720X

Gary Kenneth Hulse: https://orcid.org/0000-0002-7907-0233

Comments

Reece, A. S., & Hulse, G. K. (2024). Key insights into cannabis‐cancer pathobiology and genotoxicity. Addiction Biology, 29(11). https://doi.org/10.1111/adb.70003

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Link to publisher version (DOI)

10.1111/adb.70003