A Comprehensive Review of the Impact of Chromium Picolinate on Testicular Steroidogenesis and Antioxidant Balance.

Low testosterone (T) levels are a major cause of male infertility, as this hormone is crucial for several processes throughout the entire male reproductive tract. Leydig cells (LC) produce T through testicular steroidogenesis. Disrupted LC function can hinder steroid production and fertility. Among the factors that affect steroidogenesis, endocrine-disrupting chemicals (EDCs) raise concerns, as they disturb hormonal signaling. Chromium is classified as an EDC, and its main forms are hexavalent (Cr(VI)) and trivalent chromium (Cr(III)). While Cr(III) is controversially regarded as an essential metal, its compound Cr(III) picolinate (CrPic3) is used as a nutritional supplement due to its antidiabetic and antioxidant properties. This review aims to identify the possible effects of CrPic3 on testicular steroidogenesis and thus, on male fertility. The detriments caused by CrPic3 in LC include the inhibition of enzymes involved in steroidogenesis, and, as in other cells, the induction of mutagenesis and apoptosis. Remarkably, CrPic3 impacts male fertility through the alteration of reactive oxygen species (ROS), T levels, and sperm parameters (sperm motility and abnormal sperm count). However, gaps and inconsistencies exist in the literature concerning its effects on male fertility. Thus, further research is imperative to comprehend the underlying mechanisms of CrPic3 in the physiological processes relevant to male fertility, ensuring the supplement's safety for use by men.

Impact of Chromium Picolinate on Leydig Cell Steroidogenesis and Antioxidant Balance Using an In Vitro Insulin Resistance Model.

Leydig cells (LCs) play a pivotal role in male fertility, producing testosterone. Chromium (III) picolinate (CrPic3), a contentious supplement with antidiabetic and antioxidant properties, raises concerns regarding male fertility. Using a rodent LC line, we investigated the cytotoxicity of increasing CrPic3 doses. An insulin resistance (IR) model was established using palmitate (PA), and LCs were further exposed to CrPic3 to assess its antioxidant/antidiabetic activities. An exometabolome analysis was performed using 1H-NMR. Mitochondrial function and oxidative stress were evaluated via immunoblot. Steroidogenesis was assessed by quantifying androstenedione through ELISA. Our results uncover the toxic effects of CrPic3 on LCs even at low doses under IR conditions. Furthermore, even under these IR conditions, CrPic3 fails to enhance glucose consumption but restores the expression of mitochondrial complexes CII and CIII, alleviating oxidative stress in LCs. While baseline androgen production remained unaffected, CrPic3 promoted androstenedione production in LCs in the presence of PA, suggesting that it promotes cholesterol conversion into androgenic intermediates in this context. This study highlights the need for caution with CrPic3 even at lower doses. It provides valuable insights into the intricate factors influencing LCs metabolism and antioxidant defenses, shedding light on potential benefits and risks of CrPic3, particularly in IR conditions.

Reemergence of H3N8 Equine Influenza A virus in Chile, 2018.

A new outbreak of equine Influenza A virus (IAV) was reported in Chile in January 2018, 6 years after its last report in 2012. Equine IAV was detected by rtRT-PCR, followed by virus isolation and full genome sequencing. Genetic characterization of equine IAV classified the virus within clade 1 of the Florida sublineage. Although this is the same sublineage that caused an outbreak in Chile in 2012, the virus has a high similarity to other cocirculating viruses that were recently identified in Europe and Asia. The Chilean 2018 equine influenza (EI) outbreak was caused by an H3N8 strain circulating globally that spread through horse movements.

Avian influenza in Chile: a successful experience.

Avian influenza (AI) was diagnosed in May 2002 for the first time in Chile and South America. The epidemic was caused by the highly pathogenic AI (HPAI) virus subtype H7N3 that emerged from a low pathogenic virus. The index farm was a broiler breeder, located in San Antonio, V Region, which at the time was a densely populated poultry area. Stamping of 465,000 breeders, in 27 sheds, was immediately conducted. Surveillance activities detected a second outbreak, 1 wk later, at a turkey breeding farm from the same company. The second farm was located 4 km from the index case. Only 25% of the sheds were infected, and 18,500 turkeys were destroyed. In both outbreaks, surveillance zones and across-country control measures were established: prediagnosis quarantine, depopulation, intensive surveillance, movement control, and increased biosecurity. Other measures included cleaning, disinfection, and controlling the farms with sentinels to detect the potential presence of the virus. Zoning procedures were implemented to allow the international trade of poultry products from unaffected areas. Positive serologic results to H5N2 virus also were detected in other poultry farms, but there was no evidence of clinical signs or virus isolation. Epidemiological investigation and laboratory confirmation determined that positive serology was related to a contaminated imported batch of vaccine against inclusion body hepatitis. All actions taken allowed the control of the epidemic, and within 7 mo, Chile was free of AI. Epidemic and control measures that prevented further spread are described in this article, which illustrates the importance of a combination of control measures during and after an outbreak of AI. This study is a good example of how veterinary services need to respond if their country is affected by HPAI.