Heavy metals, sperm functional parameters and their association with male infertility

Introducción. La exposición ambiental a metales pesados, como el As, Al, Cr, Mn, Fe, Co, Ni, Cu, Zn, Se, Mo, Cd, Sn, Sb, W, Tl, Pb y U induce a efectos perjudiciales en la salud reproductiva, suprimiendo la motilidad de los espermatozoides al alterar el sistema antioxidante espermático. Objetivo.  Discutir la exposición a metales pesados y su relación con parámetros funcionales de los espermatozoides asociados a la infertilidad masculina. Metodología. Es un estudio con enfoque cualitativo, de diseño no experimental, transversal y descriptivo. Se emplearon bases de datos como Lens, Scopus, Scielo, PubMed y Elsevier para identificar las publicaciones utilizando palabras claves y operadores booleanos. Resultados. Mediante revisión bibliográfica se logró interpretar los efectos que causan los metales pesados en la salud reproductiva masculina. Conclusión.  Se evidencia que la exposición prolongada a ciertos  metales pesados altera la función testicular, lo que conduce a una mayor fragmentación del ADN, alteraciones en la morfología, motilidad y concentración del esperma, incrementando así la infertilidad en el varón.Introduction. Environmental exposure to heavy metals, such as As, Al, Cr, Mn, Fe, Co, Ni, Cu, Zn, Se, Mo, Cd, Sn, Sb, W, Tl, Pb and U induce harmful effects on health reproductive by suppressing sperm motility and altering the sperm antioxidant system. Objetive. Discuss exposure to heavy metals and its relationship with functional parameters of spermatozoa associated with male infertility. Methodology. It is a study with a qualitative approach, non-experimental, cross-sectional and descriptive design. Databases such as Lens, Scopus, Scielo, PubMed and Elsevier were used to identify publications using keywords and Boolean operators.  Results. Through a bibliographic review, it was possible to interpret the effects caused by heavy metals on male reproductive health. Conclusion. It is evident that prolonged exposure to certain heavy metals alters testicular function, which leads to greater DNA fragmentation, alterations in sperm morphology, motility and concentration, thus increasing infertility in men

Comparación de criterios diagnósticos del síndrome metabólico en un Centro de Atención Primario Rural

Objective: To compare the diagnostic criteria for metabolic syndrome based on the NCEP/ATP-III, ALAD and IDF/NHLBI/AHA definitions based on its prevalence in a population aged 18-65 years in a rural primary care center during the period 2021. Methods: Descriptive observational, non-experimental, with a sample of 267 individuals. Results: It was found that there was a predominance of the male sex, which ranged between 27-69 years; in addition, 89.8% had a normal BMI. The prevalence was 59.2% under IDF/NHLBI/AHA, followed by ALAD with 41.9% and 33.7% NCEP/ATP-III. Likewise, moderate concordance was observed between NCEP/ATP-III and IDF /NHLBI/AHA and low concordance between NCEP/ATP-III and ALAD; ALAD and IDF /NHLBI/AHA. Conclusion: Metabolic syndrome should be assessed under more specific and adaptive criteria for the population at regional level, in order to provide relevant data for future studies.Objetivo: Comparar los criterios de diagnóstico del síndrome metabólico en base a las definiciones NCEP/ATP-III, ALAD y IDF/NHLBI/AHA a partir de su prevalencia en una población de 18-65 años de un centro de atención primario rural durante el periodo 2021. Método: Observacional descriptivo, no experimental, cuya muestra estuvo constituida por 267 individuos. Resultados: Detallando que se evidenció un predominio del sexo masculino, el cual oscilaba entre los 27-69 años; además que el 89,8% presentaba un IMC normal. La prevalencia fue del 59,2% bajo IDF /NHLBI/AHA, seguido de ALAD con 41,9% y 33,7% NCEP/ATP-III. Así mismo, se observó una concordancia moderada entre NCEP/ATP-III y IDF /NHLBI/AHA y escasa entre NCEP/ATP-III y ALAD; ALAD y IDF /NHLBI/AHA. Conclusión: El síndrome metabólico debe ser valorado bajo criterios más específicos y adaptativos para la población a nivel regional, con el fin de proporcionar datos pertinentes para futuros estudios

The Hallmarks of Cervical Cancer: Molecular Mechanisms Induced by Human Papillomavirus

Human papillomaviruses (HPVs) and, specifically, high-risk HPVs (HR-HPVs) are identified as necessary factors in the development of cancer of the lower genital tract, with CaCU standing out as the most prevalent tumor. This review summarizes ten mechanisms activated by HR-HPVs during cervical carcinogenesis, which are broadly associated with at least seven of the fourteen distinctive physiological capacities of cancer in the newly established model by Hanahan in 2022. These mechanisms involve infection by human papillomavirus, cellular tropism, genetic predisposition to uterine cervical cancer (CaCU), viral load, viral physical state, regulation of epigenetic mechanisms, loss of function of the E2 protein, deregulated expression of E6/E7 oncogenes, regulation of host cell protein function, and acquisition of the mesenchymal phenotype

Molecular iodine inhibits the expression of stemness markers on cancer stem-like cells of established cell lines derived from cervical cancer

Abstract Background Cancer stem cells (CSC) are characterized by deregulated self-renewal, tumorigenicity, metastatic potential, aberrant stemness signaling pathways, resistance to conventional therapy, and the ability to give rise to a progeny of proliferating cells that constitute the bulk of tumors. Targeting CSC will provide novel treatments for cancer. Different investigations have focused on developing complementary approaches that involve natural compounds that decrease chemo-resistance and reduce the side effects of conventional therapies. Since, it has been reported that molecular iodine (I2) exhibits antineoplastic effects and decreases tumor progression in some cancer models, we evaluated the potential effect of I2 on cell cultures enriched in cervical cancer stem-like cells. Methods HeLa and SiHa cervical cancer cells were treated with 200uM I2 for 24 h. After time, cells were cultured in CSC-conditioned medium (cervospheres) and viability assays were performed. Following, tumorigenic capabilities in cervospheres treated with I2 were evaluated in NOD/SCID mice. HeLa monolayer cells untreated and their respective cervosphere cells treated or untreated with 200 μM of I2 for 24 h were xenotransplanted subcutaneously at different amounts and mice were monitored for at least 2 months. Results In the present study, monolayer and CSC-enriched cultures (cervospheres) from cervical cancer-derived cell lines, HeLa and SiHa, showed that 200uM I2 supplementation inhibits proliferation of both and decreased their tumorigenic capacity, in vivo. This antineoplastic effect of I2 was accompanied by diminished expression of stemness markers including CD49f, CK17, OCT-4, NANOG, SOX2, and KLF4, as well as increased expression and activation of PPARγ receptors. Conclusions All this data led us to suggest a clinical potential use of I2 for targeting CSC and improve current treatments against cervical cancer

CDH1 and SNAI1 are regulated by E7 from human papillomavirus types 16 and 18

A common characteristic of cancer types associated with viruses is the dysregulated expression of the CDH1 gene, which encodes E‑cadherin, in general by activation of DNA methyltransferases (Dnmts). In cervical cancer, E7 protein from high risk human papillomaviruses (HPVs) has been demonstrated to interact with Dnmt1 and histone deacetylase type 1 (HDAC1). The present study proposed that E7 may regulate the expression of CDH1 through two pathways: i) Epigenetic, including DNA methylation; and ii) Epigenetic‑independent, including the induction of negative regulators of CDH1 expression, such as Snail family transcriptional repressor Snai1 and Snai2. To test this hypothesis, HPV16‑ and HPV18‑positive cell lines were used to determine the methylation pattern of the CDH1 promoter and its expression in association with its negative regulators. Different methylation frequencies were identified in the CDH1 promoter in HeLa (88.24%) compared with SiHa (17.65%) and Ca Ski (0%) cell lines. Significant differences in the expression of SNAI1 were observed between these cell lines, and an inverse association was identified between the expression levels of SNAI1 and CDH1. In addition, suppressing E7 not only increased the expression of CDH1, but notably decreased the expression of SNAI1 and modified the methylation pattern of the CDH1 promoter. These results suggested that the expression of CDH1 was dependent on the expression of SNAI1 and was inversely associated with the expression of E7. The present results indicated that E7 from HPV16/18 regulated the expression of CDH1 by the two following pathways in which Snai1 is involved: i) Hypermethylation of the CDH1 promoter region and increasing expression of SNAI1, as observed in HeLa; and ii) Hypomethylation of the CDH1 promoter region and expression of SNAI1, as observed in SiHa. Therefore, the suppression of CDH1 and expression of SNAI1 may be considered to be biomarkers of metastasis in uterine cervical cancer.The present study received additional support of the Fundación Miguel Alemán, A.C. to AGC. PRC received a fellowship from Programa de Movilidad Internacional de Estudiantes de la Coordinación de Estudios de Posgrado (CEP‑UNAM) during his doctoral stay at the Universidad Autónoma de Madrid (UAM).Peer reviewe