Could Licorice prevent Bisphenol A-Induced Biochemical, Histopathological and Genetic Effects in the Adult Male Albino Rats?

Abstract

Bisphenol A (BPA) is an ecological estrogenic endocrine disruptor used commonly in polycarbonate plastics. This study aimed to investigate the biochemical, histopathological and genetic effects of BPA at different doses and to evaluate the protective role of licorice against such effects. Thirty Wistar male albino rats were divided into five groups administered BPA daily at 2.4 µg/kg and 500 mg/kg orally with or without licorice (150 mg/kg) for 4 weeks. The results revealed that the high toxic dose decreased GSH, SOD and catalase levels and increased MDA level significantly. Serum TNF-α, testosterone and testicular cholesterol levels were significantly decreased while serum alkaline phosphatase was significantly increased. Histopathological changes were observed in testes, lungs and stomach. Alteration in the expression of NF-κB1 gene in lung occurred. These results suggested that BPA induced oxidative stress; resulted in its complication in the examined rats and treatment with licorice alleviated the toxicity induced by BPA.

Curcumin ameliorated low dose-Bisphenol A induced gastric toxicity in adult albino rats

“…BPA molecules leak from food and beverage containers to food and drinks due to the exposure of polycarbonate products to high temperatures or reaction with acidic or basic components 2 . Therefore, BPA and its metabolites have been found in about 92.6% of human bodies 3 .…”

Disturbance in Some Fertility Biomarkers Induced and Changes in Testis Architecture by Chronic Exposure to Various Dosages of Each of Nonylphenol or Bisphenol A and Their Mix

“…According to Jung et al [ 47 ], oxidant generation increased NF-B activation, which increased TNF levels and caused tissue injury. NF-κB leads to nuclear translocation, which regulates specific cytokine genes such as TNF-alpha [ 48 ]. BPA can modify different transcriptional factors, such as Sp1 (specificity protein 1), that affect the combining site of NF-κB and hence change the transcriptional capacity of NF-κB [ 49 ].…”