RESUMO
Resumen El síndrome de Turner (ST) es causado por la ausencia del segundo cromosoma sexual, dando lugar a individuos con fenotipo femenino. Se presenta en 1/2,500 recién nacidas vivas y se estima que solo el 1% de los embriones con ST logran llegar al término de su gestación. Estas pacientes presentan baja estatura, infertilidad, enfermedades cardiacas, renales y autoinmunes. Estudios han revelado alteraciones celulares y moleculares que explican la alta mortalidad en la etapa prenatal, complicaciones obstétricas y comorbilidades en estas pacientes. El objetivo de este estudio fue revisar el conocimiento actual sobre el desarrollo de embriones con ST y su impacto en la salud de las pacientes. Se consideró la literatura científica actualizada. Se han reportado diversas alteraciones celulares y moleculares en etapas prenatales en embriones con ST que impactan en la salud de estas pacientes. La comprensión de estos mecanismos nos permitirá brindar una mejor atención obstétrica que se verá reflejada hasta la vida adulta de estas.
Abstract Turner syndrome (TS) is caused by the absence of the second sex chromosome, giving rise to individuals with a female phenotype. It occurs in 1/2,500 live newborns, and it is estimated that only 1% of embryos with TS manage to reach the end of their gestation. These patients have short stature, infertility, cardiac, renal, and autoimmune diseases. Studies have revealed cellular and molecular alterations that explain the high mortality in the prenatal stage, obstetric complications, and comorbidities. The objective of this study was to review the current knowledge about the development of embryos with TS and its impact on the health of patients. The updated scientific literature was reviewed. Various cellular and molecular alterations have been reported in prenatal stages in embryos with TS, which have an impact on the health of these patients. The understanding of these mechanisms will allow us to provide better obstetric care that will be reflected until their adult life.
RESUMO
Cadmium is a metal that can affect the male reproductive process, possibly leading to infertility. In contrast, beta-caryophyllene (BC) is a sesquiterpene that has shown antigenotoxic, anticancer, and antioxidant properties. Therefore, the aim of the present study was to determine the protective effect of BC against the deleterious effects of cadmium chloride (CC) on various mouse testicular and sperm parameters. We tested three doses of BC (20, 200, and 400 mg/kg) given before and during exposure to 3 mg/kg CC (six days after a single administration). Our results show significant alleviation of the damage induced by CC after the three doses of BC. Regarding the sperm concentration and morphology, the protection with the high dose was complete, and regarding sperm mobility and viability, the protection was more than 74%. In the comet assay, the highest dose showed a reduction of 92.5% in the damage induced by CC, and regarding the number of micronuclei in the spermatids, the reduction was 83.3%. In the oxidative evaluation, regarding sperm lipoperoxidation, the improvement was complete with the high dose, and in the ABTS.+ test, the improvement in the response to the BC high dose was 26.3%. Regarding testicular lipoperoxidation and protein oxidation, the protective effects of the high BC dose were 87.6% and 89.9%, respectively. We also found that BC protected against the histological and morphometric alterations induced by CC. Therefore, our study clearly demonstrates the beneficial, chemopreventive effect of BC against the mouse sperm and testicular alterations induced by CC.