Effect of the Egyptian propolis on the hepatic antioxidant defense and pro-apoptotic p53 and anti-apoptotic bcl2 expressions in aflatoxin B1 treated male mice

Alm-Eldeen, Abeer A.; Basyony, Mohammed; El‐Fiky, N.; Ghalwash, Mohamed M.

doi:10.1016/j.biopha.2016.12.084

Cited by 35 publications

(22 citation statements)

References 27 publications

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“…Bcl-2 exerts its anti-apoptotic activity via binding of the activated Bax effector to prevent mitochondrial outer membrane permeabilization (MOMP) in healthy hepatocytes. However, decreased Bcl-2 protein levels were found in hepatocytes exposed to AFs (Liao et al, 2014;Chen et al, 2016;Alm-Eldeen et al, 2017;Bock and Tait, 2020). Bax dimers form higher-order multimers that generate lipid pores within the outer mitochondrial membrane (OMM), which causes MOMP and the release of intermembrane space contents, such as cytochrome c (cyt c).…”

Section: Afs Damage Mitochondria To Initiate Various Cellular Injury Pathways Afs Induce the Destruction And Dysfunction Of Mitochondriamentioning

confidence: 99%

Contamination of Aflatoxins Induces Severe Hepatotoxicity Through Multiple Mechanisms

et al. 2021

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Aflatoxins (AFs) are commonly contaminating mycotoxins in foods and medicinal materials. Since they were first discovered to cause “turkey X” disease in the United Kingdom in the early 1960s, the extreme toxicity of AFs in the human liver received serious attention. The liver is the major target organ where AFs are metabolized and converted into extremely toxic forms to engender hepatotoxicity. AFs influence mitochondrial respiratory function and destroy normal mitochondrial structure. AFs initiate damage to mitochondria and subsequent oxidative stress. AFs block cellular survival pathways, such as autophagy that eliminates impaired cellular structures and the antioxidant system that copes with oxidative stress, which may underlie their high toxicities. AFs induce cell death via intrinsic and extrinsic apoptosis pathways and influence the cell cycle and growth via microribonucleic acids (miRNAs). Furthermore, AFs induce the hepatic local inflammatory microenvironment to exacerbate hepatotoxicity via upregulation of NF-κB signaling pathway and inflammasome assembly in the presence of Kupffer cells (liver innate immunocytes). This review addresses the mechanisms of AFs-induced hepatotoxicity from various aspects and provides background knowledge to better understand AFs-related hepatoxic diseases.

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Section: Afs Damage Mitochondria To Initiate Various Cellular Injury Pathways Afs Induce the Destruction And Dysfunction Of Mitochondriamentioning

confidence: 99%

Contamination of Aflatoxins Induces Severe Hepatotoxicity Through Multiple Mechanisms

et al. 2021

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“…Research has shown that propolis possesses antimicrobial, anti-inflammatory, immune-stimulatory, antiviral and hepatoprotective activities. These properties have been mostly ascribed to flavonoids, a group of natural compounds contained in propolis (25)(26)(27)(28)(29)(30)(31)(32). It is noteworthy that both in vitro and in vivo studies have recently documented the anticancer activity of propolis, as well as its mechanism of action in relation to the phytochemical composition (33)(34)(35)(36).…”

Section: Introductionmentioning

confidence: 99%

Flavonoids, bioactive components of propolis, exhibit cytotoxic activity and induce cell cycle arrest and apoptosis in human breast cancer cells MDA-MB-231 and MCF-7 – a comparative study

Kabała‐Dzik

Rzepecka‐Stojko

Kubina

et al. 2018

Cell Mol Biol (Noisy-le-grand)

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Breast cancer is one of the most common causes of mortality in women. Flavonoids, among other compounds, are bioactive constituents of propolis. In this comparative study, we investigated the effects of flavonoids apigenin (API), genistein (GEN), hesperidin (HES), naringin (NAR) and quercetin (QUE) on the proliferation, apoptosis, and cell cycle of two different human cancer cells-MDA-MB-231, estrogen-negative, and MCF-7, estrogen-positive receptor breast carcinoma cells. Many cytotoxic reports of flavonoids were performed by MTT assay. However, it's reported that MTT is reduced in metabolically active cells and yields an insoluble purple formazan, which indicates that obtained cytotoxic results of flavonoids could be inconsistent. Cell viability was measured by NR, neutral red assay, while the percentage of apoptotic cells and cell cycle arrest were determined by flow cytometry and Muse cell cycle assay, respectively. The results showed a high dose-dependent effect in cell viability tests. IC 50 values were as follows (MCF-7/MDA-MB-231, for 48 h, in µM): 9.39/50.83 for HES, 25.19/88.17 for API, 40.26/333.51 for NAR, 49.49/47.50 for GEN and 95.12/130.10 for QUE. Flavonoid-induced apoptosis was dose-and time-dependent, for both cancer cell lines, though flavonoids were more active on MCF-7 cells. The flavonoids also induced cell cycle arrest in cancer cells.

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“…The data were subjected to statistical analysis by using Graph Pad Prism 5 statistical analysis program. The test type was Dunnett's multiple comparison test (P < 0.05) which accepted as significant [13][14].…”

Section: Discussionmentioning

confidence: 99%

L-Carnitine ameliorates Cisplatin-induced testicular toxicity in rats

Alm-Eldeen

Masoud

Darwesh

et al. 2020

Delta Journal of Science

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Aim: To evaluate the effect of cisplatin on testes of male rats and to evaluate the possible curative effect of L-carnitine as an antioxidant. Methods: 18 male Albino Wistar rats were equally divided into three groups. Group I: control; Group II: cisplatin (7.5 mg/kg) for a single intraperitoneal (IP) injection; Group III cisplatin + 250 mg/kg/day of L-carnitine. Administration of L-carnitine by oral gavage started one day after cisplatin injection and was continued for 14 consecutive days. The rats were euthanized and the left testes were fixed in formaldehyde fixative for histopathological examination and morphometric analysis. The right testes were kept for biochemical tests to evaluate the levels of malondialdahyde (MDA) and reduced glutathione (GSH). Results: Cisplatin-induced impairment of spermatogenesis leading to a decreased in the testicular and gonadal organs weight, a decline in the sperms number, an increase in MDA level and a decrease in GSH level. Histological damage like degeneration, necrosis, arrest of spermatogenesis, congestion, and a decrease in the diameter of the seminiferous tubules were also observed. The rats that received cisplatin and L-carnitine showed non-significant changes in the testicular and gonadal organ weight comparing with the control rats and restored the control level of MDA and GSH. L-carnitine ameliorates the histological changes caused by cisplatin. Seminiferous tubules showed as normal with a non-significant change in their diameter. Conclusion: The findings of this study suggest that cisplatin induced testicular toxicity and L-carnitin could ameliorate this toxicity.

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Effect of the Egyptian propolis on the hepatic antioxidant defense and pro-apoptotic p53 and anti-apoptotic bcl2 expressions in aflatoxin B1 treated male mice

Cited by 35 publications

References 27 publications

Contamination of Aflatoxins Induces Severe Hepatotoxicity Through Multiple Mechanisms

Contamination of Aflatoxins Induces Severe Hepatotoxicity Through Multiple Mechanisms

Flavonoids, bioactive components of propolis, exhibit cytotoxic activity and induce cell cycle arrest and apoptosis in human breast cancer cells MDA-MB-231 and MCF-7 – a comparative study

L-Carnitine ameliorates Cisplatin-induced testicular toxicity in rats

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