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Oxidative stress plays a crucial role in the development of type 2 diabetes and the associated microvascular and cardiovascular complications. In the study, we have investigated the effects of Heinsia crinita (H. crinita) extracts on lipid peroxidation and oxidative stress responses using diabetic rats. Type 2 diabetes was induced with 10 % fructose/40 mg/kg body weight streptozotocin (STZ). H. crinita extract was administered at 200 and 400 mg/kg body weight twice daily for 21 days, in addition to metformin (MET: 500 mg/kg body weight) control. Molecular docking analysis was performed to determine the binding affinity of H. crinita extracts to the DNA binding domains of peroxisome proliferator-activated receptor (Ppar) and retinoid x receptor (Rxr) protein crystal structures, showing different binding affinities for putative active compounds from the plant. Fasting blood glucose (FBG), body and organ weight changes were determined showing that H. crinita extract induced an anti-hyperglycemic effect in the treated animals, with changes (either decrease or increase) in liver and kidney weights. A decrease in mRNA expression of peroxisome proliferator-activated receptors (ppar), sterol regulatory element-binding protein 1 (srebp-1c), liver x-receptor (lxr), retinoid x receptors (rxr), cytochrome p45041 (cyp4a1) and acyl-CoA oxidase (acox1) in diabetic animals were observed, compared to the control. A dose-specific decrease or increase in antioxidant enzymes (superoxide dismutase: SOD, catalase: CAT, reduced glutathione: GSH, glutathione peroxidase: GPx) transcripts and activity levels were also observed. We also observed exposure-specific decrease or increase of malondialdehyde (MDA) levels. Our data suggested that H. crinita extract possesses protective effects against diabetes-induced oxidative stress. These effects might be attributed to their binding and activation of nuclear receptors, indicating their cellular mode of action that is comparable to MET.

Landfills and dumpsites are the final point of solid waste deposition and management in developing countries due to lack of recycling methods. Herein, we have investigated the occurrence, polymer composition and characterization of plastic pollution at the Lemna solid waste dumpsite, Calabar Nigeria. A total of 21 plastics were sampled and categorized into 10 representative plastic types for effective identification and characterization. The plastic categories were PET bottles, LDPE, PP, HDPE, PS tray, PVC fiber and PVC others. PET bottles were the most abundant (28.5%), followed by PP > LDPE > HDPE, while PS trays, PVC fiber and PVC others were the least prevalent plastics at the dumpsite. FT-IR analysis showed that only 5 different plastics polymers (PP, PET, PE, PVC, and PS) were identified and characterized, out of the 10 plastics categories collected. However, PP and PET were the most abundant plastic polymers at the dumpsite consisting of 33.3- and 28.6%, respectively, and reflecting their widespread application in domestic and household packaging products. PS was the least abundant plastic (4.8%) polymer. We used the density gradient separation techniques and recovered only three (3) plastic polymer types from soil at the dumpsite, namely - PET, PS, and PP with sizes >5mm in diameter and indicating macroplastics. Given that plastics are vectors of contaminants of legacy and emerging concern, their continuous deposition at dumpsites represent a significant environmental, human and wildlife health issue of concern.

In the present study, we have investigated liver lipid homeostasis and corresponding changes in transcript and functional product levels in A/J mice exposed to environmental relevant concentration of per- and polyfluoroalkyl substances (PFAS) mixture. Mice were fed environmentally relevant concentrations of a PFAS mixture during a period of 10 weeks. The concentrations of the 8 individual PFAS in the mixture were chosen based on measured concentrations in earthworms at a Norwegian skiing area. Our data show high liver accumulation of ∑PFAS in exposed mice, which paralleled significant elevation in body weight and hepatosomatic index (HSI) of male mice. UPC2 -MS/MS analysis in both positive and negative mode, respectively, indicated significant differences between control and exposure groups in the liver of exposed mice. Principal component analysis (PCA) of the features revealed separation of control and exposure groups in both sexes. From the significantly differential 207 lipids, only 72 were identified and shown to belong to eight different lipid classes. PCA of fatty acids (FAs) profile showed a clear separation between control and PFAS exposure groups in both female and male mice, with differential abundant levels of 5 and 4 hydrolyzed FAs, respectively. Transcript and protein analysis of genes associated with lipid homeostasis (ppar-α and β, lxr-α and β, rxr, fasn and srebp) showed that PFAS exposure produced sex- and individual response related alterations. Glutathione reductase (Gr) activity showed exposure-related changes in both female and male mice, compared with controls. Overall, the present study has demonstrated changes in lipid metabolism after PFAS exposure, showing that PFAS accumulation in the liver resulted to hepatotoxic effects, potential interference with membrane lipid profile and homeostasis, and oxidative stress. Given the structural similarity with FAs, interaction between PFAS and nuclear receptors such as PPARs may have severe consequences for general health and physiology in exposed animals and humans.

We studied molecular effects (RNAseq and qPCR) of first feeding prey types (copepods or rotifers/Artemia) on skeletal muscle myogenesis and growth dynamics (proliferation, differentiation), metabolism (glycolysis, gluconeogenesis, oxidative phosphorylation), and antioxidant defense system (production/regulation of reactive oxygen species (ROS) in cod (Gadus morhua) larval skeletal muscle. Larval somatic growth rates were significantly higher in copepod fed larvae, although shifts in gene expressions related to muscle growth dynamics between hypertrophy and hyperplasia and generation and regulation of ROS mostly occurred around 5-, 10-, and 15-mm standard length (SL) for both groups. Gene expression for cell membrane proteins (such as nox1 and igf1r) peaked at 7 mm SL in all larvae, corresponding with increased ROS expressions in cod muscle during the exponential stratified hyperplasia phase from 7 mm SL. Expression for muscle differentiation (mef2a) occurred continuously (strongest from 10 mm SL). Expressions for muscle proliferation (pcna) and hydrogen peroxide (H2O2) generation (sod1 and sod2) occurred in the 5 - 15 mm SL range, peaking at 10 mm SL in all larvae. A downregulation of sod1 and sod2 in skeletal muscle from 15 mm SL indicated the first response of the defense antioxidant system. Gene expressions related to glucose metabolism (slc2A11, pfk, fpb2, ldha) was 3 - 10 times higher in copepod-fed larvae than in rotifer/Artemia-fed larvae between 7 – 10 mm (live prey period). Copepods move faster than rotifers, and cod larvae will also gradually increase their active swimming periods, due to less viscous forces. Active swimming during the strongest muscle stratified hyperplasia phase (7 – 10 mm SL) could promote a better delivery and transport across the muscle membrane and intracellular flux through glycolysis and oxidative phosphorylation and would contribute to the observed earlier and more effective glucose metabolism in the larvae fed copepods. We suggest that active swimming is an important factor promoting cod larval muscle growth, especially during the strongest muscle hyperplasia phase between 7 and 10 mm SL. The rapid movements of copepods and better nutritional composition could play important roles in stabilizing ROS levels, promoting high swimming activities and enhancing long-term muscle growth in cod.

Abstract We examined the potential for ultrasound as a noninvasive tool for maturation monitoring in Atlantic salmon (Salmo salar) males. Ultrasound examination and measurements were compared to common practices for maturation monitoring such as gonadosomatic index (GSI), sex hormone analysis, and histological analysis of spermatogenesis. There were significant correlations (R2 = 0.68, P

In the present study, the biotransformation and oxidative stress responses in relation to chemical burden in the liver of male and female Nile crocodiles--Crocodylus niloticus--from a commercial crocodile farm passively exposed to various anthropogenic aquatic pollutants was investigated. In general, the data showed that male crocodiles consistently produced higher biotransformation and oxidative stress responses compared to females. Relationships between these responses and concentrations of aliphatic hydrocarbons and polycyclic aromatic hydrocarbons (PAHs) were also observed. Specifically, the catalytic assays for EROD and BROD (not PROD and MROD) showed sex-differences between male and female crocodiles and paralleled immunochemically determined CYP1A and CYP3A protein levels; the relatively similar levels of PAHs in both sexes suggest an estrogen-mediated reduction of this pathway in females. The antioxidant system exhibited higher levels in male crocodiles with slight or significant higher values for catalase (CAT), glutathione reductase (GR), glutathione peroxidases-H2O2 (GPx-H2O2), glutathione peroxidases-Cu (GPx-Cu), total antioxidant capacity towards peroxyl radicals (TOSC-ROO) and hydroxyl radicals (TOSC-HO), total glutathione (GSH) and malondialdehyde (MDA). On the other hand, the activities of acyl-CoA oxidase (AOX) and glutathione S-transferases (GST) were significantly higher in females. Principal component analysis (PCA) produced significant groupings that revealed correlative relationships (both positive and negative) between biotransformation/oxidative stress variables and liver PAHs and aliphatic hydrocarbon burden. The overall results suggest that these captive pre-slaughter crocodiles exhibited adverse exposure responses to anthropogenic aquatic contaminants with potentially relevant effects on key cellular pathways, and these responses may be established as relevant species biomarkers of exposure and effects in this endangered species.

The relative importance of environmental hypoxia due to global climate change on organismal ability to adapt to chemical insult and/or mechanisms of these responses is not well understood. Therefore, we have studied the effects of combined exposure to perfluorooctane sulfonamide (PFOSA) and chemically induced hypoxia on membrane lipid profile and homeostasis. Primary salmon hepatocytes were exposed to PFOSA at 0, 25 and 50 µM singly or in combination with either cobalt chloride (CoCl2: 0 and 150 µM) or deferroxamine (DFO: 0 and 100 µM) for 24 and 48 h. CoCl2 and DFO were used to induce cellular hypoxia because these two chemicals have been commonly used in animal experiments for this purpose and have been shown to increase hypoxia-inducible factor 1-alpha (HIF-1α) and vascular endothelial growth factor (VEGF) levels. Fatty acid (FA) profiles were determined by GC-MS, while gene expression patterns were determined by quantitative PCR. Hypoxic condition was confirmed with time-related increases of HIF-1α mRNA levels in CoCl2 and DFO exposed cells. In general, significant alterations of genes involved in lipid homeostasis were predominantly observed after 48 h exposure. Gene expression analysis showed that biological responses related to peroxisome proliferation (peroxisome proliferator-activated receptors (PPARs) and acyl coenzyme A (ACOX)) and FA desaturation (Δ5- and Δ6-desaturases: FAD5 and FAD6, respectively) and elongation (FAE) were elevated slightly by single exposure (i.e. either PFOSA, CoCl2 or DFO exposure alone), and these responses were potentiated in combined exposure conditions. Principal component analysis (PCA) showed a clustering of peroxisome proliferation responses at transcript levels and FA desaturation against membrane FAs levels whose changes were explained by PFOSA and chemically induced hypoxia exposures. Overall, our data show that most of the observed responses were stronger in combined stressor exposure conditions, compared to individual stressor exposure. In general, our data show that hypoxia may, singly or in combination with PFOSA produce deleterious health, physiological and developmental consequences through the alteration of membrane lipid profile in organisms.