Acetoxy-4-methylcoumarins confer differential protection from aflatoxin B1-induced micronuclei and apoptosis in lung and bone marrow cells

Raj, Hanumantharao G.; Kohli, Ekta; Rohil, Vishwajeet; Dwarakanath, Bilikere S.; Parmar, Virinder S.; Malik, Smita; Adhikari, Jawahar Singh; Tyagi, Yogesh Kumar; Goel, Sanjay; Gupta, Kshitij; Bose, Mridula; Olsen, Carl Erik

doi:10.1016/s1383-5718(01)00176-0

Cited by 45 publications

(20 citation statements)

References 19 publications

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“…Several studies indicated that AFB 1 was able to induce apoptosis in hepatocytes, lung and bone marrow cells, or human bronchial epithelial cells [36,37,38]. In our study, through flow cytometer method and TUNEL assay, an increased apoptotic splenocytes was observed in AFB 1 groups, which revealed one mechanism of AFB 1 -induced immunosuppression.…”

Section: Discussionsupporting

confidence: 64%

Protective Effects of Sodium Selenite against Aflatoxin B1-Induced Oxidative Stress and Apoptosis in Broiler Spleen

Wang

Shu

Peng

et al. 2013

IJERPH

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The aim of this study was to investigate the possible protective role of sodium selenite on aflatoxin B1-induced oxidative stress and apoptosis in spleen of broilers. Two hundred one-day-old male broilers, divided into five groups, were fed with basal diet (control group), 0.3 mg/kg AFB1 (AFB1 group), 0.3 mg/kg AFB1 + 0.2 mg/kg Se (+Se group I), 0.3 mg/kg AFB1 + 0.4 mg/kg Se (+Se group II) and 0.3 mg/kg AFB1 + 0.6 mg/kg Se (+Se group III), respectively. According to biochemical assays, AFB1 significantly decreased the activities of glutathione peroxidase, total superoxide dismutase, glutathione reductase, catalase and the level of glutathione hormone, while it increased the level of malondialdehyde. Moreover, AFB1 increased the percentage of apoptosis cells by flow cytometry and the occurrence of apoptotic cells by TUNEL assay. Simultaneous supplementation with sodium selenite restored these parameters to be close to those in control group. In conclusion, sodium selenite exhibited protective effects on AFB1-induced splenic toxicity in broilers by inhibiting oxidative stress and excessive apoptosis.

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Section: Discussionsupporting

confidence: 64%

Protective Effects of Sodium Selenite against Aflatoxin B1-Induced Oxidative Stress and Apoptosis in Broiler Spleen

Wang

Shu

Peng

et al. 2013

IJERPH

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“…In our study, increased apoptotic splenocytes were observed in the AFB-contaminated groups by flow cytometry, and this result was in agreement with the histological observations, which showed that increased nuclear debris was present in the spleens of chicken exposed to AFB contaminated diets. Previous report showed that AFB 1 was able to induce apoptosis in hepatocytes, bone marrow cells and lung cells, or human bronchial epithelial cells [30,31,32]. These results partly revealed the mechanisms of AFB-induced immunosuppression.…”

Section: Discussionmentioning

confidence: 55%

Histological Lesions, Cell Cycle Arrest, Apoptosis and T Cell Subsets Changes of Spleen in Chicken Fed Aflatoxin-contaminated Corn

Peng

Zhang

Bai

et al. 2014

IJERPH

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The purpose of this study was to evaluate the effects of corn naturally contaminated with aflatoxin B1 and aflatoxin B2 on pathological lesions, apoptosis, cell cycle phases and T lymphocyte subsets of spleen, and to provide an experimental basis for understanding the mechanism of aflatoxin-induced immunosuppression. A total of 900 COBB500 male broilers were randomly allocated into five groups with six replicates per group and 30 birds per replicate. The experiment lasted for 6 weeks and the five dietary treatments consisted of control, 25% contaminated corn, 50% contaminated corn, 75% contaminated corn and 100% contaminated corn groups. The histopathological spleen lesions from the contaminated corn groups was characterized as congestion of red pulp, increased necrotic cells and vacuoles in the splenic corpuscle and periarterial lymphatic sheath. The contaminated corn intake significantly increased relative weight of spleen, percentages of apoptotic splenocytes, induced cell cycle arrest of splenocytes, increased the percentages of CD3+CD8+ T cells and decreased the ratios of CD3+CD4+ to CD3+CD8+. The results suggest that AFB-induced immunosuppression maybe closely related to the lesions of spleen.

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“…DAMC up-regulates the expression and activity of anti-oxidant protein thioredoxin (TRX) in the peripheral blood mononuclear cells (PBMCs), accompanied by profound reduction in the levels of intracellular reactive oxygen species (ROS) levels thereby, minimising oxidative stress50. Accumulating evidences suggest that DAMC and other PAs lower Aflatoxin B 1 (a potent carcinogen)-mediated micronuclei induction and afford protection against stress-induced DNA damage in normal lung and BM51. The potential of DAMC in stimulating angiogenesis by augmenting the levels of vascular endothelial growth factor (VEGF) has been recently demonstrated50.…”

mentioning

confidence: 99%

Mitigation of radiation-induced hematopoietic injury by the polyphenolic acetate 7, 8-diacetoxy-4-methylthiocoumarin in mice

Venkateswaran

Shrivastava

Agrawala

et al. 2016

Sci Rep

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Protection of the hematopoietic system from radiation damage, and/or mitigation of hematopoietic injury are the two major strategies for developing medical countermeasure agents (MCM) to combat radiation-induced lethality. In the present study, we investigated the potential of 7, 8-diacetoxy-4-methylthiocoumarin (DAMTC) to ameliorate radiation-induced hematopoietic damage and the associated mortality following total body irradiation (TBI) in C57BL/6 mice. Administration of DAMTC 24 hours post TBI alleviated TBI-induced myelo-suppression and pancytopenia, by augmenting lymphocytes and WBCs in the peripheral blood of mice, while bone marrow (BM) cellularity was restored through enhanced proliferation of the stem cells. It stimulated multi-lineage expansion and differentiation of myeloid progenitors in the BM and induced proliferation of splenic progenitors thereby, facilitating hematopoietic re-population. DAMTC reduced the radiation-induced apoptotic and mitotic death in the hematopoietic compartment. Recruitment of pro-inflammatory M1 macrophages in spleen contributed to the immune-protection linked to the mitigation of hematopoietic injury. Recovery of the hematopoietic compartment correlated well with mitigation of mortality at a lethal dose of 9 Gy, leading to 80% animal survival. Present study establishes the potential of DAMTC to mitigate radiation-induced injury to the hematopoietic system by stimulating the re-population of stem cells from multiple lineages.

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Acetoxy-4-methylcoumarins confer differential protection from aflatoxin B1-induced micronuclei and apoptosis in lung and bone marrow cells

Cited by 45 publications

References 19 publications

Protective Effects of Sodium Selenite against Aflatoxin B1-Induced Oxidative Stress and Apoptosis in Broiler Spleen

Protective Effects of Sodium Selenite against Aflatoxin B1-Induced Oxidative Stress and Apoptosis in Broiler Spleen

Histological Lesions, Cell Cycle Arrest, Apoptosis and T Cell Subsets Changes of Spleen in Chicken Fed Aflatoxin-contaminated Corn

Mitigation of radiation-induced hematopoietic injury by the polyphenolic acetate 7, 8-diacetoxy-4-methylthiocoumarin in mice

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