Berenice Venegas

Chronic hyperammonemia (HA) secondary to liver dysfunction is associated with cognitive impairment, oxidative stress, and neuroinflammation, particularly in hippocampal regions involved in learning and memory. This exploratory study evaluated the effects of sodium phenylbutyrate (PBA) on behavior and on biochemical and molecular changes in a rat model of CCl₄-induced HA. Male Wistar rats were randomly distributed into five groups: CTRL (control), COV (corn oil vehicle) + SSI (isotonic saline solution), HA + SSI, COV + PBA, and HA + PBA. At the end of the administration periods, locomotor activity and recognition memory were evaluated with the Open-Field Test (OFT) and Novel-Object Recognition Test (NORt). HA induced significant increases in plasma and hippocampal ammonia and glutamine levels, accompanied by hepatic dysfunction. These alterations were associated with elevated lipid peroxidation, nitrite levels, disruption of antioxidant defenses, and increased proinflammatory cytokines in the hippocampus. In addition, HA + SSI animals showed reduced BDNF (Brain-Derived Neurotrophic Factor) and NT-3 (Neurotrophin-3) levels and impaired behavioral performance. PBA administration reduced ammonia accumulation, improved redox balance (pro- and antioxidant levels), attenuated the hippocampal proinflammatory cytokine profile, and restored neurotrophin levels. These effects were accompanied by improvement in locomotor and cognitive performance. In conclusion, our results indicate that PBA attenuates systemic and hippocampal alterations induced by chronic HA.

In this study, we evaluated the effects of intrabursal administration of cabergoline and N‐acetylcysteine on ovarian hyperstimulation syndrome (OHSS) in an immature rat model. The study assessed body, ovarian, and uterine weights, as well as the concentrations of vascular endothelial growth factor A (VEGF‐A). Moreover, levels of MDA, 4‐HDA, and nitrites were assessed in ovarian homogenates, and vascular permeability was quantified in the peritoneal cavity. Ovarian morphology was characterized using histology and hematoxylin–eosin staining, determining the count of ovarian follicles and corpus luteum. Our results demonstrated a significant increase in lipoperoxidation, nitrite levels, and VEGF‐A concentrations in the OHSS group compared to the control group. These biochemical alterations corroborate the successful induction of OHSS in the experimental model. Direct injection into the ovarian bursa resulted in reduced vascular permeability and VEGF‐A levels, suggesting that the effects of cabergoline are predominantly ovarian. Particularly, cabergoline did not significantly alter other parameters such as ovarian weight, lipoperoxidation, nitrite levels, or morphology. Conversely, low concentrations of N‐acetylcysteine (25–50 µg/kg) significantly reduced ovarian and uterine weights, VEGF‐A levels, and vascular permeability. Interestingly, this dose–response relationship was not observed at higher NAC concentrations (100–200 μg/kg), suggesting a potential threshold beyond which NAC loses efficacy in these specific parameters. Our results suggest that the localized administration of N‐acetylcysteine shows promise as a therapeutic strategy for OHSS by modulating key parameters associated with the syndrome. These promising results warrant further investigation into its mechanisms and efficacy, potentially expanding therapeutic options for OHSS management.

Aeromonas es un género bacteriano reportado como patógeno emergente; debido a su capacidad de generar enfermedades infecciosas que afectan el sistema gastrointestinal, el circulatorio y algunos tejidos blandos de individuos inmunocomprometidos, adultos mayores e infantes. También, Aeromonas se comporta como un patógeno oportunista de mamíferos y peces, y posee diversos factores de virulencia. Este género prolifera en diversos ambientes como el suelo, agua y diferentes hospederos. La presente revisión bibliográfica tiene como objetivo describir los procesos metabólicos y genéticos que le confieren al género Aeromonas la resistencia a antibióticos, la capacidad de formar biopelícula, los genes regulados por el Quorum Sensing (QS) y la transferencia horizontal de genes. Además, de discutir algunas características que posicionan a la infección por Aeromonas como un problema potencial de salud pública. La revisión exhaustiva se realizó en las bases de datos del Centro Nacional de Información Biotecnológica (NCBI) y del Instituto Multidisciplinario de Publicaciones Digitales (MDPI), del 2017 a la fecha y se consideraron los siguientes criterios de búsqueda: factores de virulencia, resistencia a antibióticos formación de biopelícula y transferencia horizontal de genes. La investigación indicó que Aeromonas presenta varios factores de virulencia extracelulares, enzimáticos y estructurales; es resistente a antibióticos como betalactámicos, tetraciclinas y macrólidos y presenta varios genes que le confieren esta resistencia; asimismo, el género tiene la capacidad de formar biopelícula y posee tres sistemas de QS.

Las plantas purificadoras de agua que carecen de un adecuado sistema de control de calidad pueden generar problemas de salud pública. El objetivo de este estudio fue examinar la calidad microbiológica del agua proveniente de pequeñas plantas purificadoras de la ciudad de Puebla, así como, determinar la existencia de bacterias Aeromonas sp y Pseudomonas sp, y caracterizar si presentan un fenotipo patógeno oportunista. Se recolectaron 70 muestras de garrafones de agua de 25 establecimientos. La cuantificación bacteriana se realizó mediante el método de goteo en placa. Se comprobaron los géneros microbianos mediante análisis bioquímico. En las cepas que mostraron discrepancia se utilizó la identificación molecular con base a secuencias parciales del gen 16S rRNA para confirmar su especie y se les evaluaron sus características de patogenicidad: multirresistencia a antibióticos, producción de biopelícula y actividad hemolítica. El 40 % de las plantas purificadoras no cumplieron con la calidad microbiológica del agua para consumo humano. El 41.4 % de los garrafones de agua muestreados incumplió la normativa, presentando coliformes totales 35.7 %, Pseudomonas 30 %, Enterococcus faecalis 8.6 % y bacterias coliformes fecales el 5.7 %. Se obtuvieron 56 aislados, provenientes de los 29 garrafones contaminados; 10 de ellos se caracterizaron molecularmente, resultando 7 aislados relacionados con especies diferentes de P. aeruginosa y 3 con especies de Aeromonas. De los aislados de Pseudomonas, 5 presentaron resistencia a 2 familias de antibióticos y 2 mostraron multirresistencia. El 36 % de los 10 aislados produjeron hemólisis y biopelícula. Dos cepas de Aeromonas mostraron resistencia a Cefalosporina 3a generación pero no produjeron hemólisis. Los 10 aislados analizados fueron clasificados como no patógenos. Es necesario un seguimiento sanitario más estricto para lograr el cumplimiento de las normas nacionales e internacionales relacionadas con el consumo de agua purificada, para evitar dañar la salud de los consumidores.

Cadmium (Cd) is a heavy metal classified as a carcinogen whose exposure could affect the function of the central nervous system. Studies suggest that Cd modifies neuronal morphology in the hippocampus and affects cognitive tasks. The oxidative stress pathway is proposed as a mechanism of toxicity. However, this mechanism is not precise yet. This study aimed to evaluate the effect of Cd administration on oxidative stress markers in the male rat's hippocampus. Male Wistar rats were divided into (1) control (drinking water) and (2) treatment with Cd (32.5 ppm of cadmium chloride (CdCl₂) in water). The Cd was administered for 2, 3, and 4 months. The results show that the oral administration of CdCl₂ increased the concentration of Cd in plasma and hippocampus, and this response is time‐dependent on its administration. Likewise, it caused an increase in lipid peroxidation and nitrosative stress markers.Moreover, it increased reactive astrogliosis and antioxidant enzyme activity. Consequently, the progression of the oxidative response exacerbated neurodegeneration in hippocampal cells. Our results suggest that Cd exposure induces a severe oxidative response that contributes critically to hippocampal neurodegeneration. It is suggested that exposure to Cd increases the risk of developing neurological diseases, which contributes to a decrease in the quality of life of the human and the environment in which it lives.

In the aging process, the brain presents biochemical and morphological alterations. The neurons of the limbic system show reduced size dendrites, in addition to the loss of dendritic spines. These disturbances trigger a decrease in motor and cognitive function. Likewise, it is reported that during aging, in the brain, there is a significant decrease in neurotrophic factors, which are essential in promoting the survival and plasticity of neurons. The carboxyl‐terminal fragment of the heavy chain of the tetanus toxin (Hc‐TeTx) acts similarly to neurotrophic factors, inducing neuroprotection in different models of neuronal damage. The aim here, was to evaluate the effect of Hc‐TeTx on the motor processes of elderly mice (18 months old), and its impact on the dendritic morphology and density of dendritic spines of neurons in the limbic system. The morphological analysis in the dendrites was evaluated employing Golgi‐Cox staining. Hc‐TeTx was administered (0.5 mg/kg) intraperitoneally for three days in 18‐month‐old mice. Locomotor activity was evaluated in a novel environment 30 days after the last administration of Hc‐TeTx. Mice treated with Hc‐TeTx showed significant changes in their motor behavior, and an increased dendritic spine density of pyramidal neurons in layers 3 and 5 of the prefrontal cortex in the hippocampus, and medium spiny neurons of the nucleus accumbens (NAcc). In conclusion, the Hc‐TeTx improves the plasticity of the brain regions of the limbic system of aged mice. Therefore, it is proposed as a pharmacological alternative to prevent or delay brain damage during aging.

Metabolic syndrome (MS) is a health problem that is characterized by body fat accumulation, hypertension, dyslipidemia, and hyperglycemia; recently, it has been demonstrated that MS also damages memory processes. The first‐line drug in the treatment of MS and type 2 diabetes mellitus is metformin, which is an antihyperglycemic agent. This drug has been shown to produce neuroprotection and to improve memory processes. However, the mechanism involved in this neuroprotection is unknown. A 90‐day administration of metformin improved the cognitive processes of rats with MS as evaluated by the novel object recognition test, and this finding could be explained by an increase in the neuronal spine density and spine length. We also found that metformin increased the immunoreactivity of synaptophysin, sirtuin‐1, AMP‐activated protein kinase, and brain‐derived neuronal factor, which are important plasticity markers. We conclude that metformin is an important therapeutic agent that increases neural plasticity and protects cognitive processes. The use of this drug is important in the minimization of the damage caused by MS.

Background: Polycystic ovary syndrome is characterized by hyperactivity of the ovarian sympathetic nervous system, increases in the content and release of norepinephrine, as well as decreases in the number of β-adrenoreceptors. In the present study, β-adrenoreceptors in the ovaries of rats with polycystic ovary syndrome were blocked and analyzed the resultant effects on ovulation, hormone secretion and the enzymes responsible for the synthesis of catecholamines. Methods: At 60 days of age, vehicle or estradiol valerate-treated rats were injected with propranolol [10^− 4 M] into the ovarian bursas on oestrus day. The animals were sacrificed on the next day of oestrus, and the ovulation response, the steroid hormone levels in the serum and the immunoreactivity of tyrosine hydroxylase and dopamine β-hydroxylase in the ovaries were measured. Results: In animals with the induction of polycystic ovary syndrome and β-adrenoreceptor blocking, ovulation was restored in more than half of the animals and resulted in decreased hyperandrogenism with respect to the levels observed in the estradiol valerate-treated group. Tyrosine hydroxylase and dopamine β-hydroxylase were present in the theca cells of the growing follicles and the interstitial gland. Injection of propranolol restored the tyrosine hydroxylase and ovarian dopamine β-hydroxylase levels in rats with polycystic ovary syndrome induction. Conclusions: The results suggest that a single injection into the ovarian bursas of propranolol, a nonselective antagonist of β-adrenoreceptor receptors, decreases the serum testosterone concentration and the formation of ovarian cysts, improving the ovulation rate that accompanies lower levels of tyrosine hydroxylase and dopamine β-hydroxylase in the ovary.

The injection of estradiol valerate in female rats induces polycystic ovary syndrome, which is characterized by polycystic ovaries, anovulation, and hyperandrogenism. These characteristics have been associated with an increase in the ovarian concentration of norepinephrine, which occurs before establishing the polycystic ovary syndrome. The bilateral section of the superior ovarian nerve restores ovarian functions in animals with polycystic ovary syndrome. The superior ovarian nerve provides norepinephrine and vasoactive intestinal peptide to the ovary. An increase in the activity of both neurotransmitters has been associated with the development of polycystic ovary syndrome. The purpose of the present study was analyzed the participation of the noradrenergic nervous system in the development of polycystic ovary syndrome using guanethidine as a pharmacological tool that destroys peripheral noradrenergic nerve fibers. Fourteen-day old female rats of the CIIZ-V strain were injected with estradiol valerate or vehicle solution. Rats were randomly allotted to one of three guanethidine treatment groups for denervation: 1) guanethidine treatment at age 7 to 27-days, 2) guanethidine treatment at age 14 to 34- days, and 3) guanethidine treatment at age 70 to 90- days. All animals were sacrificed when presenting vaginal oestrus at age 90 to 94-days. The parameters analyzed were the number of ova shed by ovulating animals, the ovulation rate (i.e., the numbers of ovulating animals/the numbers of used animals), the serum concentration of progesterone, testosterone, oestradiol and the immunoreactivity for tyrosine hydroxylase enzyme. All data were analyzed statistically. A p-value of less than 0.05 was considered significant. Our results show that the elimination of noradrenergic fibers before the establishment of polycystic ovary syndrome prevents two characteristics of the syndrome, blocking of ovulation and hyperandrogenism. We also found that in animals that have already developed polycystic ovary syndrome, sympathetic denervation restores ovulatory capacity, but it was not as efficient in reducing hyperandrogenism. The results of the present study suggest that the noradrenergic fibers play a stimulant role in the establishment of polycystic ovary syndrome.

An important worldwide health problem as the result of current lifestyle is metabolic syndrome (MS). It has been shown that MS induced by a high‐calorie diet (HCD) in rats produces cognitive deterioration in the novel object recognition test (NORt) and decreases synaptic connections and dendritic order in the hippocampus and temporal cortex. However, it is unknown whether MS induced by an HCD participates in the cognitive process observed with the injection of Aβ_1–42 into the hippocampus of rats as a model of Alzheimer disease (AD). The induction of MS in rats produces a deterioration in NORt; however, rats with MS injected with Aβ_1–42 show a major deterioration in the cognitive process. This event could be explained by the increment in the oxidative stress in both cases studied (MS and Aβ_1–42): together, the hippocampus and temporal cortex produce an enhancer effect. In the same way, we observed an increment in interleukin‐1β, TNF‐α, and GFAP, indicative of exacerbated inflammatory processes by the combination of MS and Aβ_1–42. We can conclude that MS might play a key role in the apparition and development of cognitive disorders, including AD. We propose that metabolic theory is important to explain the apparition of cognitive diseases.