Maternal impacts of pre-conceptional glyphosate exposure.

Maternal glyphosate (GLY) impacts remain unclear despite associations between urinary GLY and birth outcomes. Whether maternal pre-conceptional GLY exposure would have phenotypic and molecular impacts in the dam and offspring was tested. Female C57BL6 mice (6 wk) were exposed to saline (CT; n = 20) or GLY (2 mg/kg; n = 20) per os five d per week for 20 wk.

Evaluation of Two Phenotypic Methods for the Detection of Plasmid-Mediated AmpC β-Lactamases among Enterobacteriaceae Isolates.

 AmpC β-lactamases are cephalosporinases that confer resistance to cephalothin, cefazolin, cefoxitin, penicillin, and β-lactamase inhibitor-β-lactam combinations. Even though the AmpC resistance is reported, but the accurate occurrence of AmpC β-lactamases in members is still unknown. Techniques to identify AmpC producers are still evolving but not yet optimized for the clinical laboratory.

The Aryl hydrocarbon receptor mediates reproductive toxicity of polychlorinated biphenyl congener 126 in rats.

Polychlorinated biphenyls (PCBs) are endocrine disrupting chemicals with documented, though mechanistically ill-defined, reproductive toxicity. The toxicity of dioxin-like PCBs, such as PCB126, is mediated via the aryl hydrocarbon receptor (AHR) in non-ovarian tissues. The goal of this study was to examine the uterine and ovarian effects of PCB126 and test the hypothesis that the AHR is required for PCB126-induced reproductive toxicity.

Ovarian mitochondrial and oxidative stress proteins are altered by glyphosate exposure in mice.

Glyphosate (GLY) usage for weed control is extensive. To investigate ovarian impacts of chronic GLY exposure, female C57BL6 mice were orally administered saline as vehicle control (CT) or GLY at 0.25 (G0.

Absence of glyphosate-induced effects on ovarian folliculogenesis and steroidogenesis.

Glyphosate (GLY) is an herbicidal active ingredient and both in vitro and in vivo studies suggest that GLY alters ovarian function. To determine if a chronic GLY exposure model affected steroidogenesis or folliculogenesis in vivo, postnatal day 42 C57BL6 female mice were orally delivered vehicle control (saline) or GLY (2 mg/Kg) from a pipette tip five days per week for either five or ten weeks. Mice were euthanized at the pro-estrus stage of the estrous cycle.

Developmental origins of ovarian disorder: impact of maternal lean gestational diabetes on the offspring ovarian proteome in mice†.

Gestational diabetes mellitus (GDM) is an obstetric disorder affecting approximately 10% of pregnancies. The four high-fat, high-sucrose (HFHS) mouse model emulates GDM in lean women. Dams are fed a HFHS diet 1 week prior to mating and throughout gestation resulting in inadequate insulin response to glucose in mid-late pregnancy.

Impact of toxicant exposures on ovarian gap junctions.

Ovarian gap junctions function to provide intercellular communication between ovarian cell types and are critical for proper ovarian function. Connexons are communication channels that are comprised of connexin (CX) proteins. Connexins can be regulated through endocrine signals, thus have dynamic expression throughout the estrous cycle.

Prolonged environment-induced hyperthermia alters autophagy in oxidative skeletal muscle in Sus scrofa.

Prolonged heat stress represents a continuing threat to human health and agricultural production. Despite the broad, negative impact of prolonged hyperthermia little is known about underlying pathological mechanisms leading to negative health outcomes, which has limited the development of etiological interventions and left clinicians and producers with only cooling and rehydration strategies. The purpose of this investigation was to determine the extent to which prolonged environment-induced hyperthermia altered autophagy in oxidative skeletal muscle in a large animal model, serving the dual purpose of accurately modeling human physiology as well as agricultural production.

Short-term heat stress results in increased apoptotic signaling and autophagy in oxidative skeletal muscle in Sus scrofa.

Prolonged environment-induced hyperthermia causes morbidities and mortality in humans and animals and appears to cause organ-specific injury and dysfunction. We have previously determined autophagic dysfunction and apoptotic signaling in oxidative skeletal muscle following prolonged hyperthermia. The aim of this investigation was to extend our knowledge regarding the early chronology of heat stress-mediated apoptotic and autophagic signaling in oxidative skeletal muscle.

Short-term heat stress altered metabolism and insulin signaling in skeletal muscle.

Heat-related complications continue to be a major health concern for humans and animals and lead to potentially life-threatening conditions. Heat stress (HS) alters metabolic parameters and may alter glucose metabolism and insulin signaling. Therefore, the purpose of this investigation was to determine the extent to which 12 h of HS-altered energetic metabolism in oxidative skeletal muscle.

Enhanced antibacterial effects of green synthesized ZnO NPs using Aristolochia indica against Multi-drug resistant bacterial pathogens from Diabetic Foot Ulcer.

Background: Increased incidence of Multi-drug resistance in microorganisms has become the greatest challenge in the treatment of Diabetic Foot Ulcer (DFU) and urges the need of a new antimicrobial agent. In this study, we determined the bactericidal effects of ZnO nanoparticles (ZnO NPs) green synthesized from Aristolochia indica against Multi-drug Resistant Organisms (MDROs) isolated from pus samples of DFU patients attending in a tertiary care hospital in South India.

Methods: ZnO NPs were characterized by UV-vis-DRS spectroscopy, Atomic Force Microscopy (AFM), Transmission Electron Microscopy (TEM) and for its zeta potential value.

Acute heat stress activated inflammatory signaling in porcine oxidative skeletal muscle.

Despite well-studied clinical manifestations, intracellular mechanisms of prolonged hyperthermic injury remain unclear, especially in skeletal muscle. Given muscle's large potential to impact systemic inflammation and metabolism, the response of muscle cells to heat-mediated injury warrants further investigation. We have previously reported increased activation of NF-B signaling and increased NF-B and AP-1-driven transcripts in oxidative skeletal muscle following 12 h of heat stress.

Heat stress causes dysfunctional autophagy in oxidative skeletal muscle.

We have previously established that 24 h of environmental hyperthermia causes oxidative stress and have implicated mitochondria as likely contributors to this process. Given this, we hypothesized that heat stress would lead to increased autophagy/mitophagy and a reduction in mitochondrial content. To address this hypothesis pigs were housed in thermoneutral (TN; 20°C) or heat stress (35°C) conditions for 1- (HS1) or 3- (HS3) days and the red and white portions of the semitendinosus collected.

Short-term heat stress alters redox balance in porcine skeletal muscle.

Heat stress contributes to higher morbidity and mortality in humans and animals and is an agricultural economic challenge because it reduces livestock productivity. Redox balance and associated mitochondrial responses appear to play a central role in heat stress-induced skeletal muscle pathology. We have previously reported increased oxidative stress and mitochondrial content in oxidative muscle following 12 h of heat stress.

Resistance training performed at distinct angular velocities elicits velocity-specific alterations in muscle strength and mobility status in older adults.

Background: The purpose of this study was to compare the effects of high and low velocity knee extension training on changes in muscle strength and mobility status in high-functioning older adults.

Methods: Twenty-six (16 female, 10 male) older adults (mean age of 65) were randomized to either 6weeks of low velocity resistance training (LVRT) performed at 75°/s or high velocity resistance training (HVRT) performed at 240°/s. Both groups performed 3 sets of knee extension exercises at maximal effort, 3 times a week.

Progressive obesity alters ovarian insulin, phosphatidylinositol-3 kinase, and chemical metabolism signaling pathways and potentiates ovotoxicity induced by phosphoramide mustard in mice.

Mechanisms underlying obesity-associated reproductive impairment are ill defined. Hyperinsulinemia is a metabolic perturbation often observed in obese subjects. Insulin activates phosphatidylinositol 3-kinase (PI3K) signaling, which regulates ovarian folliculogenesis, steroidogenesis, and xenobiotic metabolism.

Obesity alters phosphoramide mustard-induced ovarian DNA repair in mice.

Phosphoramide mustard (PM) destroys rapidly dividing cells and activates the DNA double strand break marker, γH2AX, and DNA repair in rat granulosa cells and neonatal ovaries. The effects of PM exposure on DNA damage and activation of DNA damage repair in lean and obese female mice were investigated. Wild type (lean) non agouti (a/a) and KK.

Bisphenol A-Induced Ovotoxicity Involves DNA Damage Induction to Which the Ovary Mounts a Protective Response Indicated by Increased Expression of Proteins Involved in DNA Repair and Xenobiotic Biotransformation.

Bisphenol A (BPA) is an endocrine disrupting chemical with ubiquitous human exposure. BPA causes primordial follicle loss and DNA damage in germ cells, thus we hypothesized that BPA induces ovarian DNA damage, thereby precipitating follicle loss. We also anticipated that the ovary activates DNA repair and xenobiotic biotransformation to minimize oocyte damage and/or, activate cell death signaling to deplete follicles.

Twelve hours of heat stress induces inflammatory signaling in porcine skeletal muscle.

Heat stress causes morbidity and mortality in humans and animals and threatens food security by limiting livestock productivity. Inflammatory signaling may contribute to heat stress-mediated skeletal muscle dysfunction. Previously, we discovered increased circulating endotoxin and intramuscular oxidative stress and TNF-α protein abundance, but not inflammatory signaling following 24 and 72 h of heat stress.

The ovarian DNA damage repair response is induced prior to phosphoramide mustard-induced follicle depletion, and ataxia telangiectasia mutated inhibition prevents PM-induced follicle depletion.

Phosphoramide mustard (PM) is an ovotoxic metabolite of cyclophosphamide and destroys primordial and primary follicles potentially by DNA damage induction. The temporal pattern by which PM induces DNA damage and initiation of the ovarian response to DNA damage has not yet been well characterized. This study investigated DNA damage initiation, the DNA repair response, as well as induction of follicular demise using a neonatal rat ovarian culture system.

Phosphoramide mustard exposure induces DNA adduct formation and the DNA damage repair response in rat ovarian granulosa cells.

Phosphoramide mustard (PM), the ovotoxic metabolite of the anti-cancer agent cyclophosphamide (CPA), destroys rapidly dividing cells by forming NOR-G-OH, NOR-G and G-NOR-G adducts with DNA, potentially leading to DNA damage. A previous study demonstrated that PM induces ovarian DNA damage in rat ovaries. To investigate whether PM induces DNA adduct formation, DNA damage and induction of the DNA repair response, rat spontaneously immortalized granulosa cells (SIGCs) were treated with vehicle control (1% DMSO) or PM (3 or 6μM) for 24 or 48h.

Enhanced susceptibility of ovaries from obese mice to 7,12-dimethylbenz[a]anthracene-induced DNA damage.

7,12-Dimethylbenz[a]anthracene (DMBA) depletes ovarian follicles and induces DNA damage in extra-ovarian tissues, thus, we investigated ovarian DMBA-induced DNA damage. Additionally, since obesity is associated with increased offspring birth defect incidence, we hypothesized that a DMBA-induced DNA damage response (DDR) is compromised in ovaries from obese females. Wild type (lean) non agouti (a/a) and KK.

Impact of obesity on 7,12-dimethylbenz[a]anthracene-induced altered ovarian connexin gap junction proteins in female mice.

The ovarian gap junction proteins alpha 4 (GJA4 or connexin 37; CX37), alpha 1 (GJA1 or connexin 43; CX43) and gamma 1 (GJC1 or connexin 45; CX45) are involved in cell communication and folliculogenesis. 7,12-dimethylbenz[a]anthracene (DMBA) alters Cx37 and Cx43 expression in cultured neonatal rat ovaries. Additionally, obesity has an additive effect on DMBA-induced ovarian cell death and follicle depletion, thus, we investigated in vivo impacts of obesity and DMBA on CX protein levels.

Progressive obesity alters ovarian folliculogenesis with impacts on pro-inflammatory and steroidogenic signaling in female mice.

Diet-induced obesity induces immune cell infiltration and inflammation in peri-ovarian adipose tissue and mRNA expression of inflammatory markers in ovarian tissue. Whether these changes are associated with obesity-related ovarian dysfunction remains unknown. In the present study, qRT-PCR and Western blotting techniques were used to compare mRNA and protein abundance of ovarian immune cell and inflammation markers, along with NF-kappaB and steroidogenic pathway members in normal wild-type non-agouti (a/a; lean) and lethal yellow mice (KK.

Impact of obesity on ovotoxicity induced by 7,12-dimethylbenz[a]anthracene in mice.

Insulin, elevated during obesity, regulates xenobiotic biotransformation enzymes, potentially through phosphatidylinositol 3-kinase (PI3K) signaling, in extraovarian tissues. PI3K regulates oocyte viability, follicular activation, and ovarian chemical biotransformation. 7,12-Dimethylbenz[a]anthracene (DMBA), a carcinogen and ovotoxicant, destroys all stages of follicles, leading to premature ovarian failure.