Summary: According to research, cannabis use causes cellular damage that causes DNA damage and mitochondrial damage, which increases the risk of greatly cancerous tumors. This genotoxicity can result in abnormalities, accelerated aging, and birth defects, with ability to get passed on to future generations through egg and sperm. A molecular knowledge of how cannabis affects genetic security is provided by insights from more in-depth mitochondrial research.
Important Information:
- DNA damage from hemp causes cancers and aging to progress more quickly.
- Coming generations may inherit the genotoxic effects of cannabis.
- Cannabis use and dna damage are linked by nuclear function.
Origin: Society for the Study of Addiction
A new study published in the medical journal Addiction Biology finds that cannabis use causes cellular destruction that raises the risk of greatly cancerous tumors.  ,
The report describes hemp as a “genotoxic” material because it damages a cell’s genetic data, which can lead to DNA abnormalities, accelerated aging, and cancers.  , To make matters worse, this genotoxicity may be transmitted via broken egg and sperm to the cannabis person’s descendants, making the risk of hemp use trans-generational.
Researchers from The University of Western Australia have made a connection between new studies showing that mitochondria function causes genetic injury, which results in increased rates of cancer, accelerated aging, and baby defects, and established knowledge that cannabis use inhibits the production of cellular energy by inhibiting mitochondria.
The , Science , analyses were not conducted in the framework of hemp use, however, they provide mechanistic insights into some studies about cannabis use that were not originally well understood, such as that hemp causes both nuclear and biological damage.
Taken together, the article , in Addiction Biology , put older historical research about cannabis into context and suggests that cannabis-related genotoxic damage may be all around us — even if we largely do n’t see it.
Co-author Dr. Stuart Reece comments:” The link we’ve described between cannabis use and genotoxicity has far-reaching consequences. This recent study demonstrates how the effects of cannabis use can be passed down through generations.  ,
This shift should change the discussion about legalizing marijuana from a personal choice to one that might involve multiple generations.
About this news about cancer and epigenetics
Author: Jean O’Reilly
Source: Society for the Study of Addiction
Contact: Jean O’Reilly – Society for the Study of Addiction
Image: The image is credited to Neuroscience News
Original Research: Closed access.
By Stuart Reece and al.,” Micronscratching from oxidative damage.” Science
Open access.
Stuart Reece and colleagues ‘” Key Insights into Cannabis-Cancer Pathobiology and Genotoxicity” Addiction Biology
Abstract
Oxative damage causes nuclear collapse.
INTRODUCTION
Chromosomal instability, a hallmark of aggressive cancers, is characterized by the presence of micronuclei, which are cytosolic rupture-prone structures that contain entire chromosomes or chromosome arms. A major component of tumor progression is the irreversible collapse of micronuclear envelopes.
The cytosol is exposed to the encapsulated DNA by micronuclear collapse, which causes chromosomal rearrangements and epigenetic changes that contribute to tumor heterogeneity and drug resistance.
Micronuclear rupture also activates inflammatory signaling pathways that reshape the tumor immune microenvironment, promoting metastasis. Despite its importance, the underlying mechanisms of micronuclear collapse are unclear.
RATIONALE
Cellular functions and organismal viability depend on maintaining the integrity of the nuclear membrane. What cellular safeguards are compromised in nuclear membrane integrity in micronuclei, yet it is not clear what causes this.
We argued that the differences in membrane stability between micronuclei and primary nuclei may be due to their inherent differences. For instance, micronuclei are 5- to 20-fold smaller than the primary nucleus.
Secondly, they possess abnormal nuclear envelopes, as evidenced by aberrant nuclear pore function and reduced lamin B1 levels. In addition, once ruptured, micronuclear envelopes are seldom repaired.
RESULTS
Reactive oxygen species ( ROS ) are involved in the investigation of how previous observations and our findings contributed to the discovery that micronuclear envelope rupture occurs due to the aberrant interaction between micronuclei and mitochondria. In fact, damaged micronuclei were more likely to be compared to intact ones when their rates of micronuclear rupture were altered by ROS levels.
The endosomal sorting complex, known as the endosomal sorting complex, is disrupted by subsequent proteomic analysis and genetic manipulations, leading to the discovery that ROS interferes with micronuclear integrity. The ESCRT-II I scaffolding protein, charged multivesicular body protein 7, was increased in ROS levels, promoting a noncanonical function.
CHMP7’s export was halted by ROS, which in turn caused its persistence in the micronucleus and its aberrant binding to LEM domain nuclear envelope protein 2 ( LEMD2 ), its inner nuclear membrane partner. CHMP7’s interaction with its canonical binding partners in the ESCRT-II I complex was shortened by ROS-induced cysteine oxidation. The binding of CHMP7 aggregates to LEMD2 promoted micronuclear membrane deformation and collapse.
ROS-dependent recruitment of the autophagy-related protein p62, which halted the degradation of canonical ESCRT-II I members and reduced the likelihood of a subsequent membrane repair, made this effect even more troubling. Lastly, we found that this mechanism is relevant to human tumors. Elevated levels of ROS and aberrant CHMP7 function led to complex chromosomal rearrangements, or chromothripsis, known to arise from micronuclear rupture.
Furthermore, ROS generated under hypoxia induced micronuclear rupture in a CHMP7-dependent manner. In hypoxic areas of human head and neck cancer as well as in ovarian tumors, we observed a significant increase in micronuclear rupture and CHMP7 accumulation in line with these findings.
CONCLUSION
Our findings have revealed that micronuclei and mitochondria interact pathologically and cause nuclear rupture. By implicating ROS as regulators of micronuclear integrity, this work provides a mechanistic link between ROS-inducing conditions ( such as free-radical generation and hypoxia ) and downstream processes known to arise from the presence of micronuclei, including chromosomal rearrangements, epigenetic dysregulation, and tumor-promoting inflammation.
Abstract
Key Insights into Cannabis-Cancer Pathobiology and Genotoxicity
Despite the well-known characteristics of the cannabis literature, mitochondrial stress and dysfunction have recently been demonstrated to be a potent and direct contributor to chromosomal breakage and enlargement through a variety of mechanisms.
Genotoxic damage can be anticipated to manifest in increased cancer rates, congenital anomalies, aging, and pathologies, which are becoming more prevalent in contemporary continent-wide studies.
Cannabinoid genotoxicity has been largely overlooked for decades, but it may be present everywhere thanks to the rapid aging of sperm, zygotes, foetuses, and adult organisms, which has many lines of evidence demonstrating transgenerational effects.
Indeed, the debate over legalizing marijuana is reframed by the absolute need to safeguard the genomic and epigenomic integrity of multiple generations to come as a result of this multigenerational dimension of cannabinoid genotoxicity.
