Primary cellular target responsible for dimethylnitrosamine-induced immunosuppression in the mouse

Johnson, Kirk W.; Munson, Albert E.; Holsapple, Michael P.

doi:10.1016/0162-3109(87)90026-9

Cited by 20 publications

(3 citation statements)

References 35 publications

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“…In vivo and in vitro treatments with DMN induce a broad spectrum of genotoxic effects: chromosomal aberrations (CA) in Chinese hamster V79 cells, point mutations in the Ames test and sister-chromatid exchanges (SCE) in mouse bone marrow and V79 cells [32,33]. Additional biological effects are immunosupression of murine splenocytes and hepatocytes [34,35] and cell-cycle delays in mouse maternal and fetal cells [36].…”

Section: Discussionmentioning

confidence: 99%

Protective Effect of Green Tea Against Dimethylnitrosamine Induced Genotoxicity in Mice Bone Marrow Cells~!2010-01-11~!2010-03-29~!2010-08-27~!

Al-Fify¹,

Aly²

2010

TOCJ

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Cancer is a major cause of death in the world; thus, the prevention of this disease would have a significant impact on public health. Chemoprevention is defined as natural and synthetic pharmacological (chemical) agent to disrupt the process of carcinogenesis. Green tea is a potent chemopreventive agent in many test systems and has been shown to inhibit tumor promotion and induce apoptosis. It is one of the most frequently consumed beverages in the world. Green tea polyphenolics have demonstrated antimutagenic, anticarcinogenic, antioxidant and antipromotional effects.The aim of this work is to study the protective effect of green tea extract against genotoxic damage of dimethylnitrosamine (DMN) in mice bone marrow cells.Our results demonstrated that the administration of green tea extract 24 hr before the DMN injection significantly suppressed DMN-induced chromosomal aberrations and sister chromatid exchanges. The suppression was observed 18 hr, 24 hr and 48 hr after the DMN treatment but no suppressive effect was observed at the early period (6 hr and 12 hr) after the DMN treatment. Furthermore, the suppression was observed in all doses of DMN (4, 5 and 6 mg/kg) investigated. Mice were given green tea 2 hr before the DMN injection displayed no suppressive effect.Mice were given 2% green tea extract as the sole source of drinking water for four days before sacrifice displayed significantly suppressed DMN-induced chromosomal aberrations and sister chromatid exchanges.We conclude that green tea presents significant antigenotoxic concern under the anticipated conditions of use. These results are consistent with other antigenotoxicity studies of green tea.

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Section: Discussionmentioning

confidence: 99%

Protective Effect of Green Tea Against Dimethylnitrosamine Induced Genotoxicity in Mice Bone Marrow Cells~!2010-01-11~!2010-03-29~!2010-08-27~!

Al-Fify¹,

Aly²

2010

TOCJ

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“…Johnson et al ( 1987 ) suggested that the B lymphocyte is the primary cellular target of the NDMA‐induced suppressed antibody response. This effect was found to depend on metabolic activation.…”

Section: Assessmentmentioning

confidence: 99%

“…application of NDMA (60 mg/kg bw) reduced the responsiveness to sRBC; the alteration persisted for at least 10 days. Johnson et al (1987) suggested that the B lymphocyte is the primary cellular target of the NDMAinduced suppressed antibody response. This effect was found to depend on metabolic activation.…”

Section: Reproductive Effectsmentioning

confidence: 99%

Risk assessment of N‐nitrosamines in food

Schrenk¹,

Bignami²,

Bodin³

et al. 2023

EFS2

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EFSA was asked for a scientific opinion on the risks to public health related to the presence of Nnitrosamines (N-NAs) in food. The risk assessment was confined to those 10 carcinogenic N-NAs occurring in food (TCNAs), i.e. NDMA, NMEA, NDEA, NDPA, NDBA, NMA, NSAR, NMOR, NPIP and NPYR. N-NAs are genotoxic and induce liver tumours in rodents. The in vivo data available to derive potency factors are limited, and therefore, equal potency of TCNAs was assumed. The lower confidence limit of the benchmark dose at 10% (BMDL 10 ) was 10 μg/kg body weight (bw) per day, derived from the incidence of rat liver tumours (benign and malignant) induced by NDEA and used in a margin of exposure (MOE) approach. Analytical results on the occurrence of N-NAs were extracted from the EFSA occurrence database (n = 2,817) and the literature (n = 4,003). Occurrence data were available for five food categories across TCNAs. Dietary exposure was assessed for two scenarios, excluding (scenario 1) and including (scenario 2) cooked unprocessed meat and fish. TCNAs exposure ranged from 0 to 208.9 ng/kg bw per day across surveys, age groups and scenarios. 'Meat and meat products' is the main food category contributing to TCNA exposure. MOEs ranged from 3,337 to 48 at the P95 exposure excluding some infant surveys with P95 exposure equal to zero. Two major uncertainties were (i) the high number of left censored data and (ii) the lack of data on important food categories. The CONTAM Panel concluded that the MOE for TCNAs at the P95 exposure is highly likely (98-100% certain) to be less than 10,000 for all age groups, which raises a health concern.

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Role of the transfer of metabolites from hepatocytes to splenocytes in the suppression of in vitro antibody response by dimethylnitrosamine

Kim

Yang

Johnson

et al. 1988

Biochemical Pharmacology

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Primary cellular target responsible for dimethylnitrosamine-induced immunosuppression in the mouse

Cited by 20 publications

References 35 publications

Protective Effect of Green Tea Against Dimethylnitrosamine Induced Genotoxicity in Mice Bone Marrow Cells~!2010-01-11~!2010-03-29~!2010-08-27~!

Protective Effect of Green Tea Against Dimethylnitrosamine Induced Genotoxicity in Mice Bone Marrow Cells~!2010-01-11~!2010-03-29~!2010-08-27~!

Risk assessment of N‐nitrosamines in food

Role of the transfer of metabolites from hepatocytes to splenocytes in the suppression of in vitro antibody response by dimethylnitrosamine

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