Alleviating impact of hydroethanolicMurraya koenigiileaves extract on bisphenol A instigated testicular lethality and apoptosis in mice

Abstract

Bisphenol A (BPA) is a well‐known endocrine disruptor that imposees adverse effects on male fertility via interacting with germ cells of testis. Objectives of present study were to investigate the possible protective effects of hydroethanolic Murraya koenigii leaves extract (HEMKLE) against BPA‐induced testicular damage and apoptosis in mice. Male Balb/c mice were divided into four different groups: Group I (control), Group II (HEMKLE), Group III (BPA) and Group IV (HEMKLE + BPA). Group III (BPA) showed significant decrease in sperm parameters, germ cell number along with increased lipid peroxidation (LPO) and reactive oxygen species (ROS). A significant decrease in antioxidant enzymes activity was also observed in Group III (BPA) animals. mRNA expression study revealed significant decrease in the expression of Bcl‐2 and increase in expressions of caspase‐9 and caspase‐3, thus clearly demonstrate BPA‐induced apoptosis. In addition, HEMKLE co‐administration to BPA‐treated mice showed a significant increase in sperm parameters, germ cell number, decreased levels of LPO and ROS, increased antioxidant enzymes activity in Group IV (HEMKLE + BPA). Also, mRNA expression study showed a significant increase in Bcl‐2 and decrease in caspase‐9 and caspase‐3 gene expressions in Group IV (HEMKLE + BPA). Thus, the present study suggests that HEMKLE intervention provides protection against BPA‐induced oxidative stress and apoptosis.

Selenium attenuates bisphenol A incurred damage and apoptosis in mice testes by regulating mitogen‐activated protein kinase signalling

“…Likewise, in present study, mRNA and protein expression analysis revealed a marked reduction in the expression of Bcl‐2 and an upregulation in the caspase‐9, caspase‐8 and caspase‐3 in BPA‐treated group, which demonstrate apoptosis. Previous studies also confirmed a similar trend of an increased expression of caspase‐9 and caspase‐3 upon BPA exposure (Kaur et al., 2020; Li et al., 2009; Xia et al., 2014). A study by Qian et al.…”

“…A significant decline in the activities of SOD, CAT and GSH/GSSG ratio, whereas a noticeable increase in the GST activity was observed in the BPA‐induced mice when compared to control mice, which showed toxic effects (increasing the OS) of BPA on the mice testis . Previously published reports also evidenced the BPA‐incited toxicity via disrupting the antioxidant defence system and excess ROS generation (Kaur & Sadwal, 2020; Kaur et al., 2018, 2020). However, Se supplementation restored the activities of all these in Se co‐treated group, presenting its role in eliminating free radicals, and this might be the fundamental compensatory mechanism to avoid the development of the OS.…”

“…It has been stated that BPA exposure induced the oxidative stress (OS) within body and interfere with the function of androgen receptors and male sex hormones by inducing excessive free radicals (Manfo et al., 2014). The OS created by free radicals can cause severe damage to vital components of the cell and also deregulate the inherent repair mechanism, which ultimately leads to cell apoptosis (Kaur & Sadwal, 2020; Kaur et al., 2020). Adverse consequences of BPA exposure on spermatogenesis comprise a marked decline in the weight of prostate and testes, and decreased thickness as well as diameter of seminiferous tubules (Kaur et al., 2020; Qiu et al., 2013).…”

Antioxidant effect of Vitamin E on the male rat reproductive system by a high oral dose of Bisphenol-A

“…1 One of the known reason of BPA toxicity is the induction of oxidative stress, 3 which disrupts the male and female reproductive systems. 6 Many studies have shown that BPA can decreases the levels of antioxidant enzymes 7,8 although, can increases malondialdehyde (MDA) levels 7,8 and other oxidative stress factors, 9,10 In following that, it can degenerate germinal epithelium, 11,12 besides, it causes degradation in the sperm quality and quantity, 11,12 testosterone levels, as well as, spermatogenesis. 13 It is undeniable that the oxidative stress property of BPA is one of the most important reasons for its toxicity, therefore, in this study, Vitamin E (VE) was used as a potent antioxidant to neutralize the free radicals created by BPA.…”

Role of Antioxidants in Alleviating Bisphenol A Toxicity

“…As another example, Murraya koenigii leaf extract exerts a protective effect in mouse orally administered BPA. M. koenigii exerts protective effects against BPA by improving sperm parameters, and decreasing lipid peroxidation and ROS levels in mouse testis [68]. Gallic acid, another natural antioxidant, is commonly found in fruits and vegetables.…”