Morphological and Cytochemical Effects of Marijuana Cigarette Smoke on Epithelioid Cells of Lung Explants from Mice

Leuchtenberger, Cecilie; Leuchtenberger, Rudolf

doi:10.1038/234227a0

Cited by 67 publications

(37 citation statements)

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“…Leuchtenberger and Leuchtenberger (1970) reported an increase in the mitotic activity in mouse 3T3 cells exposed to the gas phase of cigarette smoke. A significantly increased mitotic index in the cells was observed on exposure to a mixture of tobacco and marijuana smoke (Leuchtenberger & Leuchtenberger, 1971). A similar increase was reported by Korte, Wagner, and Obe (1981) in smoke-treated Chinese hamsters.…”

Section: Resultssupporting

confidence: 81%

Cytogenetic damage in bidi smokers

Yadav

Thakur

2000

Nicotine & Tobacco Research

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The genotoxic effects of bidi smoke were investigated in the somatic chromosomes of 45 men habituated to smoking bidi. Mitotic index (MI), chromosomal aberrations (CA), sister chromatid exchanges (SCE) and satellite associations (SA) were used as parameters. When compared with the results obtained in the blood samples from the comparable non-smoker group of men, a significant increase (p < 0.01) was noted in all the above mentioned parameters of the smoker subjects: MI (3.71-6.24), CA (0.84-3.23), SCE (3.68-7.65) and SA (5.26-11.28). A clear time-dose-effect relationship has been observed. Bidi smoke thus is both clastogenic and genotoxic for human beings.

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Section: Resultssupporting

confidence: 81%

Cytogenetic damage in bidi smokers

Yadav

Thakur

2000

Nicotine & Tobacco Research

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“…We feel that these data are widely generalizable for several reasons, including the internal consistency of results within this study, their external consistency with other studies of large datasets published internationally [ 4–9 , 17 , 18 , 55 , 86 , 87 ], the demonstration that the criteria of epidemiological causality are fulfilled (by inverse probability weighting and E -value studies), their robust mechanistic support from the cellular and molecular literature in laboratory investigations [ 24–26 , 28–30 , 168 , 169 , 177–180 ] and strong support from the preclinical prenatal cannabinoid exposure literature involving several model animal species [ 83 , 85 ].…”

Section: Discussionsupporting

confidence: 72%

Cannabinoid and substance relationships of European congenital anomaly patterns: a space-time panel regression and causal inferential study

Reece

Hulse

2022

Environmental Epigenetics

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With reports from Australia, Canada, USA, Hawaii and Colorado documenting a link between cannabis and congenital anomalies (CAs), this relationship was investigated in Europe. Data on 90 CAs were accessed from Eurocat. Tobacco and alcohol consumption and median household income data were from the World Bank. Amphetamine, cocaine and last month and daily use of cannabis from the European Monitoring Centre for Drugs and Drug Addiction. Cannabis herb and resin Δ9-tetrahydrocannabinol concentrations were from published reports. Data were processed in R. Twelve thousand three hundred sixty CA rates were sourced across 16 nations of Europe. Nations with a higher or increasing rate of daily cannabis use had a 71.77% higher median CA rates than others [median ± interquartile range 2.13 (0.59, 6.30) v. 1.24 (0.15, 5.14)/10 000 live births (P = 4.74 × 10−17; minimum E-value (mEV) = 1.52]. Eighty-nine out of 90 CAs in bivariate association and 74/90 CAs in additive panel inverse probability weighted space-time regression were cannabis related. In inverse probability weighted interactive panel models lagged to zero, two, four and six years, 76, 31, 50 and 29 CAs had elevated mEVs (< 2.46 × 1039) for cannabis metrics. Cardiovascular, central nervous, gastrointestinal, genital, uronephrology, limb, face and chromosomalgenetic systems along with the multisystem VACTERL syndrome were particularly vulnerable targets. Data reveal that cannabis is related to many CAs and fulfil epidemiological criteria of causality. The triple convergence of rising cannabis use prevalence, intensity of daily use and Δ9-tetrahydrocannabinol concentration in herb and resin is powerfully implicated as a primary driver of European teratogenicity, confirming results from elsewhere.

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“…Morishima et al (10,11) observed hypoploid metaphase cells in cultured lymphocytes obtained from marihuana users and in THC-treated lymphocytes derived from control subjects. Mouse lung cultures ex posed to marihuana smoke combined with tobacco smoke contained a statistically greater number of cells with 4N complement of DNA than cells treated exclusively with tobacco smoke (5). In studies with human lung cultures, marihuana as well as tobacco smoke resulted in variability in number and DNA content of chromosomes (6).…”

Section: Discussionmentioning

confidence: 99%

Influence of Cannabinoids on Somatic Cells <i>in vivo</i>

Zimmerman¹,

Raj²

1980

Pharmacology

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Chromosomal and nuclear aberrations in bone marrow cells were studied in hybrid mice of genotype (C57BL x C3H)F₁ following treatment with specific cannabinoids. In the subacute series, mice were treated for 5 consecutive days with Δ⁹-tetrahydrocannabinol (THC), cannabinol or cannabidiol at a dose of 10 mg/kg, the percentage of micronuclei in cannabinoid-treated mice was 3- to 5-fold greater than in the dimethyl sulfoxide controls. In the acute series, polychromatic erythrocytes were scored after a single exposure. In one acute series there was an approximately twofold increase in the incidence of micronuclei in the cannabinoid-treated mice; in the other acute series of cannabinoid-treated animals the micronuclei values were as high as 6 times the control values. Interaction between dose and frequency of exposure was assessed for THC; the number of micronuclei was affected by THC dosage, but not by frequency of exposure. Further confirmation of nuclear aberrations was obtained from assessment of bone marrow mitosis. In this limited study of mitotic cells the incidence of metaphase aberrations in cannabinoid-treated animals was 5–7 times greater than in controls.

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Morphological and Cytochemical Effects of Marijuana Cigarette Smoke on Epithelioid Cells of Lung Explants from Mice

Cited by 67 publications

References 1 publication

Cytogenetic damage in bidi smokers

Cytogenetic damage in bidi smokers

Cannabinoid and substance relationships of European congenital anomaly patterns: a space-time panel regression and causal inferential study

Influence of Cannabinoids on Somatic Cells <i>in vivo</i>

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