Attenuation of genotoxicity, oxidative stress, apoptosis and inflammation by rutin in benzo(a)pyrene exposed lungs of mice: plausible role of NF-κB, TNF-α and Bcl-2

Shahid, Ayaz; Rashid, Asif; Ali, Nemat; Hasan, Syed Kazim; Rashid, Summya; Majed, Ferial; Sultana, Sarwat

doi:10.1515/jcim-2015-0078

Cited by 38 publications

(24 citation statements)

References 64 publications

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“…ROS formation causes lipid membrane damage, which is measured by the level of MDA formed. MDA formation is the major factor causing mutation and tumor formation by forming MDA‐DNA adducts . Corresponding with the earlier findings, DMH treatment shows an increased in the level of an LPO product (MDA) .…”

Section: Discussionsupporting

confidence: 72%

Gallic acid prevents 1, 2‐Dimethylhydrazine induced colon inflammation, toxicity, mucin depletion, and goblet cell disintegration

Shree

Islam

Vafa

et al. 2020

Environmental Toxicology

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1,2-Dimethylhydrazine (DMH), an environmental toxicant specifically targets the colon. The present study was aimed to evaluate the efficacy of gallic acid (GA) against colon toxicity induced by DMH in Wistar rats. GA, a phenolic acid has numerous beneficial properties, which include antiviral, antifungal and antioxidant properties which help cells to overcome oxidative stress and balance the redox homeostasis. GA was administered orally at two doses (25 and 50 mg/kg body weight) once daily for 14 days and a single dose (40 mg/kg body weight) of DMH was administered subcutaneously on 14th day. Animals were sacrificed on the 15th day and we could find that GA at both the doses significantly ameliorates DMH-induced increased toxicity markers and also substantially increases the glutathione content level and activities of detoxifying enzymes. It also ameliorates the expression of proliferation, inflammation, apoptosis, goblet cell disintegration, and mucin depletion in the colon that was elevated upon administration of DMH. Histological alterations provide further confirmation of the protective role of GA against DMH-induced colon toxicity. The results of this study clearly indicate supplementation of GA is beneficial in ameliorating DMH-induced oxidative stress, inflammation, proliferation, apoptosis, mucin depletion, and goblet cell disintegration in colon of Wistar rats.

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Section: Discussionsupporting

confidence: 72%

Gallic acid prevents 1, 2‐Dimethylhydrazine induced colon inflammation, toxicity, mucin depletion, and goblet cell disintegration

Shree

Islam

Vafa

et al. 2020

Environmental Toxicology

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“…In conclusion, the data available so far suggest that B[a]P can trigger many, if not all, cancer hallmarks, including angiogenesis [138], inflammation [147,148], and escape to immune destruction due to immunotoxic effects of this carcinogen [149,150]. As we will detail in section 4, the mode of action of B[a]P upon several of these hallmarks seems to involve changes in H + homeostasis, as shown by our group.…”

Section: Effects On Progression Phasesupporting

confidence: 53%

Environmental carcinogenesis and pH homeostasis: Not only a matter of dysregulated metabolism

Hardonnière

Huc

Sergent

et al. 2017

Seminars in Cancer Biology

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According to the World Health Organization, around 20% of all cancers would be due to environmental factors. Among these factors, several chemicals are indeed well recognized carcinogens. The widespread contaminant benzo[a]pyrene (B[a]P), an often used model carcinogen of the polycyclic aromatic hydrocarbons' family, has been suggested to target most, if not all, cancer hallmarks described by Hanahan and Weinberg. It is classified as a group I carcinogen by the International Agency for Research on Cancer; however, the precise intracellular mechanisms underlying its carcinogenic properties remain yet to be thoroughly defined. Recently, the pH homeostasis, a well known regulator of carcinogenic processes, was suggested to be a key actor in both cell death and Warburg-like metabolic reprogramming induced upon B[a]P exposure. The present review will highlight those data with the aim of favoring research on the role of H dynamics in environmental carcinogenesis.

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“…Together, this might have potentially contributed to the genotoxic effect of CoCl 2 . The involvement of oxidative stress, inflammation, and apoptosis and their relationship with genotoxicity has been reported elsewhere . However, prolonged oxidative stress can lead to chronic inflammation which in turn might serve as a link to some chronic diseases such as cancer, diabetes and cardiovascular diseases.…”

Section: Discussionmentioning

confidence: 84%

Cobalt chloride exposure dose-dependently induced hepatotoxicity through enhancement of cyclooxygenase-2 (COX-2)/B-cell associated protein X (BAX) signaling and genotoxicity in Wistar rats

Awoyemi¹,

Okotie²,

Oyagbemi

et al. 2017

Environmental Toxicology

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Cobalt chloride (CoCl ) is one of the many environmental contaminants, used in numerous industrial sectors. It is a pollutant with deadly toxicological consequences both in developing and developed countries. We investigated toxicological impact of CoCl on hepatic antioxidant status, apoptosis, and genotoxicity. Forty Wistar rats were divided into four groups, 10 rats per group: Group 1 served as control and received clean tap water orally; Group 2 received CoCl solution (150 mg/L); Group 3 received CoCl solution (300 mg/L); and Group 4 received CoCl (600 mg/L) in drinking water for 7 days, respectively. Exposure of rats to CoCl led to a significant decline in hepatic antioxidant enzymes together with significant increase in markers of oxidative stress. Immunohistochemistry revealed dose-dependent increase in cyclooxygenase-2 and BAX expressions together with increased frequency of Micronucleated Polychromatic Erythrocytes. Combining all, CoCl administration led to hepatic damage through induction of oxidative stress, inflammation, and apoptosis.

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Attenuation of genotoxicity, oxidative stress, apoptosis and inflammation by rutin in benzo(a)pyrene exposed lungs of mice: plausible role of NF-κB, TNF-α and Bcl-2

Abstract: The findings of the present study supported the protective effect of rutin against B(a)P-induced lung toxicity and genotoxicity.

Cited by 38 publications

References 64 publications

Gallic acid prevents 1, 2‐Dimethylhydrazine induced colon inflammation, toxicity, mucin depletion, and goblet cell disintegration

Gallic acid prevents 1, 2‐Dimethylhydrazine induced colon inflammation, toxicity, mucin depletion, and goblet cell disintegration

Environmental carcinogenesis and pH homeostasis: Not only a matter of dysregulated metabolism

Cobalt chloride exposure dose-dependently induced hepatotoxicity through enhancement of cyclooxygenase-2 (COX-2)/B-cell associated protein X (BAX) signaling and genotoxicity in Wistar rats

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