cyanoginosin-lr and Metabolic-Diseases

Microcystin-LR (MC-LR) produced by cyanobacteria blooms poses a serious risk to aquatic organisms. Rice straw-derived biochar (BC) is gradually being utilized as an effective adsorbent to remove water pollutants. In the present study, the combined toxicity of MC-LR and BC on hepatic antioxidant capacity and metabolic phenotype of zebrafish (Danio rerio) were conducted due to the increasing concern of eutrophication in aquatic environments. Female zebrafish were exposed to solutions of MC-LR (10 μg/L) and BC (100 μg/L) individually and in combination for 30 days. The results indicated that sub-chronic MC-LR exposure induced oxidative stress and metabolic disorders, with a significant elevation of several amino acids, glucose as well as unsaturated fatty acids. Metabolic pathway analysis showed that the ascorbate and aldarate metabolism and biosynthesis of unsaturated fatty acids were affected under MC-LR stress. Significantly increased MDA levels along with significantly decreased CAT and GPx activities were observed in the MC-LR group. Nevertheless, MDA levels, antioxidant enzyme activities, and the relevant gene expressions (cat1, nrf2a, HO-1, keap1a) returned to baseline in the co-exposure group. These findings revealed that MC-LR resulted in metabolic disorders of protein, sugar, and lipid related to energy production, and BC could relieve MC-LR-induced metabolic disorder and oxidative stress in the liver of zebrafish. However, the potential risk of BC-induced metabolic disorder should not be neglected. Our present results highlight the potential of BC as a tool for mitigating the negative impacts of MC-LR on aquatic organisms in blooms-contaminated water.

Topics: Animals; Antioxidants; Chromatography, Liquid; Fatty Acids, Unsaturated; Female; Liver; Metabolic Diseases; Microcystins; Oryza; Tandem Mass Spectrometry; Water Pollutants, Chemical; Zebrafish

There is growing evidence that microcystins (MCs) act as hazardous materials and can disrupt the endocrine systems of animals. However, the response of thyroid function and the related energy metabolism following MCs exposure is still unknown. In the present study, mice were injected intraperitoneally (i.p.) with doses of either 5 or 20 μg/kg MC-LR for 4 weeks. We report, for the first time, that mice exposed to 20 μg/kg MC-LR showed disrupted glucose, triglyceride and cholesterol metabolism with obvious symptoms of hyperphagia, polydipsia, and weight loss. The circulating thyroid hormone (TH) levels in mice following MC-LR exposure were detected. Significantly increased free triiodothyronine (FT3) and decreased free thyroxin (FT4) were largely responsible for the physiological aberrations and metabolic disorders observed in mice after the 20 μg/kg MC-LR exposure. Increased expression of TH receptor (Trα) and mTOR expression in the brain after the 20 μg/kg MC-LR exposure suggests that the increased FT3 enhanced mTOR signaling subsequently led to hyperphagia and elevated energy expenditure in mice. Furthermore, several genes involved in glucose homeostasis and lipid metabolism, which have been identified affected by TH, were also differentially expressed after MC-LR exposure. The above results clearly showed that mice exposed to MC-LR experienced thyroid dysfunction and its downstream functional changes, and are useful to better understand the endocrine toxicity of MC-LR to mammals or even humans.

Topics: Animals; Behavior, Animal; Biomarkers; Blood Glucose; Dose-Response Relationship, Drug; Eating; Endocrine Disruptors; Energy Metabolism; Feeding Behavior; Gene Expression Regulation; Hyperphagia; Lipids; Male; Marine Toxins; Metabolic Diseases; Mice; Mice, Inbred BALB C; Microcystins; Motor Activity; RNA, Messenger; Thyroid Diseases; Thyroid Gland; Thyroxine; Time Factors; Triiodothyronine; Weight Loss