Background and Objectives: To investigate the effect of infection with human papillomavirus (HPV) or Chlamydia trachomatis (CT) and HPV + CT coinfection on sperm quality, inflammation, and the state of oxidative stress (OS) in asymptomatic infertile men. Materials and Methods: Semen samples from 84 asymptomatic military infertile men were studied. The polymerase chain reaction (PCR) was used for the molecular detection of HPV and CT. Semen parameters were analyzed according to the World Health Organization guidelines. Inflammation was evaluated by an IL-1β, IL-6, and IFN-γ enzyme-linked immunosorbent assay (ELISA) and OS by the quantification of lipid peroxidation (LPO), 8-hydroxydeoxyguanosine (8-OHdG), and total antioxidant capacity (TAC). Results: A total of 81 of the 84 (96.4%) samples were positives for the pathogens, with 55/81 (68%) being positive for HPV, 11/81 (13.5%) for CT, and 15/81 (18.5%) for HPV + CT coinfection. Seminal parameters were affected in the infected groups, including pH increases above the normal range in all groups. An abnormal sperm morphology was observed in the HPV and HPV + CT groups. Higher cytokine levels were detected in the HPV group and the highest IL-1β level was found in the HPV + CT group. No cytokines were detected in the CT group. High LPO and 8-OHdG levels were found in all groups with a lower TAC. Comparisons between groups showed the highest OS state was observed in the HPV group. Conclusions: High HPV infection or coinfection (HVP + CT) in these infertile men suggest compromising male fertility by inducing a proinflammatory state and OS. Infection with CT suggests an alteration of the state of OS by promoting an alkaline pH.

No abstract

Breast cancer (BrC) is a major health problem in women all around the world. A growing knowledge about these alterations and their associated molecular signaling pathways offers opportunities for therapeutic strategies; chemotherapy is one of the most utilized treatments; however, because of the adverse side effects and multidrug resistance that patients may present, there has been great advancement in search of new alternatives as the use of plant-derived natural compounds. This review describes information on the progress and development of cytotoxic compounds against BrC belonging to the families of flavonoids, terpenes, and alkaloids that through in vitro and in vivo studies have demonstrated to induce cellular death mainly through apoptosis, activating the intrinsic pathway. The in vitro IC 50 and the in vivo EC 50 dose-response relationship can vary depending on various factors, including the choice of cell line and/or the model used. Also, the association of some of these compounds with nanoparticles or paclitaxel with antibodies has clearly shown a potential improvement in its effect. The clinical studies that are being conducted with some of them show promising results; however, it is necessary to continue with the effort to develop new and more effective drugs against different types of BrC.Cytotoxic Effect and Mechanisms from Some In vivo models for studying plant-derived compounds in breast cancerWide varieties of animal model systems are now available to investigate plantderived compounds in different stages, such as cancer initiation, promotion progression, invasion, and metastasis. These models are also used to comprehend therapeutic response, which represents an essential step between in vitro systems and clinical studies [8,13]. The in vivo models are also used to investigate the capability of plant formulation to induce an anti-BrC effect where it is sought to optimize dose, bioavailability, administration routes, and selective delivery and reduce toxic effects, among others [8,14]. The two animal species that will be mentioned in this review are those involving mice and rats [14]; however, BrC mouse models are used in a variety of preclinical studies [13].There are different types of in vivo models of BrC, such as cell line-derived xenografts (MDA-MB-231 line) that are implanted into immunocompromised animals (cell-derived xenografts, CDX). CDX models represent a relatively homogenous mass of transformed breast epithelial cells, and depending on where the cells are inoculated, they are classified as ectopic CDX (models advanced disease only, subcutaneous injection of human tumor cells), orthotopic CDX (in mammary gland/fat pad), metastatic CDX (following tail vein or intra-cardiac injection in specific sites, i.e., bone or lung), syngeneic (mouse tissue implanted to strainmatched host) or metastasis with syngeneic model (usually fast-growing tumors and microenvironment derive from the same species, i.e., 4T1 cells), and genetically engineered mouse models (GEMMs) to address early events of tu...

Genetic factors, such as the mitochondrial DNA (mtDNA) T16189C polymorphism, have been associated with metabolic syndrome (MetS), but this association has not been studied in Mexico to date. The aim of the present study was to determine whether this polymorphism contributes to MetS in the Mexican population. We recruited 100 unrelated volunteer subjects who were divided into 2 groups: with MetS (MetS group) and without MetS (control group). All subjects were genotyped for the mtDNA T16189C polymorphism by polymerase chain reaction and sequencing. The mitochondrial T16189C polymorphism was detected in 24 (24%) of 100 subjects analyzed. The frequency of the mtDNA T16189C polymorphism was higher in the MetS group with 21 (32.3%) of 65 testing positive compared to 3 (8.5%) of 35 in the control group, indicating that this polymorphism is a probable risk factor for MetS in the Mexican population (odds ratio 5.0909, 95% CI 1.3977–18.5424, P = 0.0136). Our results may contribute to early diagnosis of MetS, which is essential for establishing changes in early stages of the disease to avoid further complications and pathologies, thereby preventing the development of type 2 diabetes and cardiovascular disease in Mexico.