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.
Abstract. The present study revealed the effects of Lycopene enriched tomato extract (LycT) on chemically induced skin cancer in mice. Skin tumors were induced by topical application of 7,12-Dimethylbenz(a)anthracene (DMBA) [500 nmol/100 ul of acetone, twice a week for two weeks] and 12-O-tetradecanoyl phorbol-13-acetate (TPA) [1.7 nmol/100 ul of acetone, twice a week for eighteen weeks] and LycT (5 mg/kg b.w.) was administered orally. Male Balb/c mice were divided into four groups (n = 15 per group): control, DMBA/TPA, LycT and LycT + DMBA/TPA. The chemopreventive response of LycT to skin tumorigenesis was evident by inhibition in tumor incidence, number, size, burden and volume in LycT + DMBA/TPA group when compared to DMBA/TPA group. This was associated with inhibition of cell proliferation in LycT + DMBA/TPA group as observed by the decrease in epidermal morphometric parameters and mRNA and protein expression of proliferating cell nuclear antigen when compared to DMBA/TPA group (p ≤ 0.05). LycT decreased (p ≤ 0.05) the mRNA and protein expression of angiogenic genes (vascular endothelial growth factor, angiopoietin-2, basic fibroblast growth factor) in LycT + DMBA/TPA group, suggesting its anti-angiogenic effects. The increase (p ≤ 0.05) in protein expression of connexin-32 and 43 in LycT + DMBA/TPA group suggests improved inter cellular communication when compared to DMBA/TPA group. Histochemical studies demonstrated that the components of extracellular matrix (fibrous proteins and mucopolysaccharides) were also modulated during skin carcinogenesis and its chemoprevention by LycT. The decrease in cell proliferation parameters and expression of angiogenesis associated genes, modulation of ECM components and increase in expression of connexins suggest that LycT improved multiple dysregulated processes during chemoprevention of skin cancer.
Doxorubicin, a chemotherapeutic drug, is known to disrupt the normal spermatogenesis by excess oxidative stress. The present study describes the curative effects of dietary supplemented selenium on doxorubicin‐induced testicular damage in mice. Four groups were included in the study: Group I(C), Group II (Se‐0.5 ppm/kg diet), Group III (Dox‐3mg/kg body weight i.p.) and Group IV (Se + Dox). We analysed microscopic sperm parameters, histopathology, testicular germ cell kinetics, oxidative stress levels, antioxidant levels and mRNA expression studies of apoptotic and stress response markers. Sperm parameters were significantly reduced in doxorubicin‐treated group. Moreover, mice treated with doxorubicin showed an elevation in oxidative stress markers as well as decreased redox ratio, and antioxidant levels were observed in Group III (Dox). However, selenium supplementation ameliorated the damage incurred by doxorubicin, by improving sperm parameters, antioxidant levels and histoarchitecture of mice testes, and decreased the oxidative stress levels. Selenium administration also reduced the levels of apoptotic caspases and stress‐activated kinases in Group IV (Se + Dox) when compared to Group III (Dox). In conclusion, selenium exhibits the curative effect against doxorubicin‐induced testicular damage in mice by attenuating stress conditions and associated apoptosis.
Being a vital micronutrient, along with a trace element, selenium (Se) protects the cells from oxidative stress (OS) in the form of selenoproteins. Bisphenol A (BPA) is a xeno‐oestrogenic compound that adversely affects the spermatogenesis process by inducing oxidative stress, which ultimately leads to male infertility. Therefore, it is hypothesised that Se could protect against BPA‐induced OS, and further germ cell death by modifying mitogen‐activated protein kinase (MAPK) signalling. Male Balb/c mice were divided into four groups: Group I (C) (0.2 ppm Se), Group II (Se) (0.5 ppm Se), Group III (BPA) (0.2 ppm Se, and BPA = 1 mg/kg orally) and Group IV (Se + BPA) (0.5 ppm Se, and BPA = 1 mg/kg bodyweight orally). Results indicated that BPA‐treated animals demonstrated a marked decrease in antioxidant enzyme activities (superoxide dismutase, catalase, redox ratio), a marked elevation in the expressions of stress‐activated kinases (c‐Jun NH2‐terminal kinase (JNK), extracellular signal‐regulated kinase (ERK) and p38) and the expressions of pro‐apoptotic markers (caspase‐9, caspase‐8 and caspase‐3). However, Se supplementation considerably restored the antioxidant enzyme activities and lowered the expressions of stress‐activated kinases, which further down‐regulated the apoptosis. Thus, Se supplementation demonstrated to be effective against BPA provoked testicular damage.
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