ABSTRACT
Fluoride induced reprotoxicity through oxidative stress-mediated reproductive cell death. Hence, the current study evaluated the importance of the MST/Nrf2/MAPK/NQO-HO1 signaling pathway in fluorosis-induced reproductive toxicity. For this purpose, the reproductive toxicity of sodium fluoride (NaF) at physiological, biochemical, and intracellular levels was evaluated. In-vivo, NaF at 100 mg/L instigated physiological dysfunction, morphological, stereological, and structural injuries in the gut-gonadal axis of fluorosis mice through weakening the antioxidant signaling, Nrf2/HO-1/NQO1signaling pathway, causing the gut-gonadal barrier disintegrated via oxidative stress-induced inflammation, mitochondrial damage, apoptosis, and autophagy. Similar trends were also observed in-vitro in the isolated Leydig cells (LCs) challenging with 20 mg/L NaF. Henceforth, activating the cellular antioxidant signaling pathway, Nrf2/HO-1/NQO1, inactivating autophagy and apoptosis, or attenuating lipopolysaccharide (LPS) can be the theoretical basis and valuable therapeutic targets for coping with NaF-induced reproductive toxicity.
Subject(s)
Antioxidants , NF-E2-Related Factor 2 , Male , Mice , Animals , Antioxidants/metabolism , NF-E2-Related Factor 2/metabolism , Kelch-Like ECH-Associated Protein 1/metabolism , Signal Transduction , Oxidative Stress , Sodium Fluoride/toxicity , ApoptosisABSTRACT
Lead (Pb) is a highly toxic heavy metal. Pb exposure could adversely affect many organs, including the male reproductive system. Oxidative stress and mitochondrial impairment play a fundamental role in the pathogenesis of Pb-induced male reproductive system injury. Taurine (TAU) is abundantly found in mammalian bodies. The positive effects of TAU on oxidative stress biomarkers and mitochondrial function have been reported. The current study evaluated the effects of TAU on Pb-induced reproductive toxicity. Mice received Pb (20 mg/kg/day; gavage, 35 consecutive days). Then, sperm indices (quality and quantity) together with sperm kinetics, sperm mitochondrial parameters, testicular and sperm oxidative stress biomarkers, testis and plasma testosterone levels, and the expression of genes involved in the steroidogenesis process have been evaluated. Pb caused significant histopathological alterations and oxidative stress in male mice's reproductive system and sperm. Moreover, significant mitochondrial function impairment was evident in sperm isolated from Pb-treated mice. Pb exposure also suppressed the expression of StAR, 17ß-HSD, CYP11A, and 3ß-HSD genes in the male gonad. It was found that TAU (500 and 1000 mg/kg) significantly improved oxidative stress biomarkers in both male gonads and gametes of Pb-treated mice. TAU also significantly restored sperm mitochondrial function and kinetics. The expression of genes involved in steroidogenesis was also higher in TAU-treated animals. These data suggest TAU as an effective agent against Pb-induced reproductive toxicity. The effects of TAU on oxidative stress markers, mitochondrial function, and the steroidogenesis process seem to play a fundamental role in its protective properties. Further studies are warranted to detect the precise protective effects of this amino acid in the reproductive system. Lead (Pb) is a toxic element that adversely affects the male reproductive system. Mitochondrial impairment and oxidative stress have a crucial role in the Pb-induced reproductive toxicity. Taurine (TAU) could considerably improve the reproductive toxicity induced by Pb via enhancing mitochondrial function and mitigating oxidative stress indices. ΔΨ, mitochondrial membrane potential; ATP, adenosine triphosphate.
Subject(s)
Lead , Taurine , Male , Mice , Animals , Taurine/pharmacology , Taurine/metabolism , Biomechanical Phenomena , Lead/toxicity , Lead/metabolism , Semen/metabolism , Spermatozoa/metabolism , Testis/metabolism , Oxidative Stress , Mitochondria/metabolism , Biomarkers/metabolism , Testosterone , Mammals/metabolismABSTRACT
The association between Cadmium and the risk of preterm birth (PTB) has remained controversial. A number of studies found a positive correlation between maternal Cd exposure and PTB; however, there are conflicting reports about this correlation. Therefore, herein we performed this meta-analysis to examine the association between maternal Cd exposure and the risk of PTB.A systematic search was conducted through PubMed, Scopus, Embase and OpenGrey from inception to May 2020 to find all eligible studies. Odds ratios (ORs) and corresponding 95% confidence intervals (CIs) were used to examine this correlation. A random-effects model was applied in this meta-analysis due to significant statistical heterogeneity among included studies.Overall, 10 eligible studies met the inclusion criteria and were included in our analysis, and results of the present meta-analysis indicated that maternal cadmium exposure is associated with the risk of PTB (OR = 1.32; 95% CI = 1.08-1.61).This meta-analysis suggests that maternal Cd exposure might be associated with the risk of PTB. Yet, large prospective studies from different ethnic populations which consider other influencing parameters are still required to confirm this finding.
Subject(s)
Premature Birth , Cadmium/toxicity , Female , Humans , Infant, Newborn , Maternal Exposure/adverse effects , Odds Ratio , Premature Birth/chemically induced , Premature Birth/epidemiology , Prospective StudiesABSTRACT
Objective: The aim of this meta-analysis was to examine the association of ApoE polymorphism with the risk of developing PE.Methods: A comprehensive search was carried out through PubMed, Scopus, and Embase. The ORs with corresponding 95% CIs were extracted. Fixed model was used for meta-analysis and in case of existing heterogeneity a random-effects model was applied.Results: Association of ApoE polymorphism with the risk of developing PE was not statistically significant (OR = 0.86, 95% CI: 0.67-1.11; OR = 0.92, 95%CI: 0.73-1.15, respectively for ε2 and ε4).Conclusion: ApoE polymorphism might not be associated with the risk of PE.
