cyanoginosin-lr and phenanthrene

Hazardous substances, such as microcystin-LR (MC-LR) and phenanthrene (Phe) are ubiquitous co-contaminants in eutrophic freshwaters, which cause harms to aquatic organisms. However, the risks associated with the co-exposure of aquatic biota to these two chemicals in the environment have received little attention. In this study, the single and mixture toxic effects of MC-LR and Phe mixtures were investigated in Daphnia magna after acute and chronic exposure. Acute tests showed that the median effective concentrations (48 h) for MC-LR, Phe and their mixtures were 13.46, 0.57 and 8.84 mg/L, respectively. Mixture toxicity prediction results indicated that the independent action model was more applicable than the concentration addition model. Moreover, combination index method suggested that the mixture toxicity was concentration dependent. Synergism was elicited at low concentrations of MC-LR and Phe exposure (≤4.04 + 0.17 mg/L), whereas antagonistic or additive effects were induced at higher concentrations. The involved mechanism of antagonism was presumably attributable to the protective effects of detoxification genes activated by high concentrations of MC-LR in mixtures. Additionally, chronic results also showed that exposure to a MC-LR and Phe mixture at low concentrations (≤50 +2 μg/L) resulted in greater toxic effects on D. magna life history than either chemical acting alone. The significant inhibition on detoxification genes and increased accumulation of MC-LR could be accounted for their synergistic toxic effects on D. magna. Our findings revealed the exacerbated ecological hazard of MC-LR and Phe at environmental concentrations (≤50 +2 μg/L), and provided new insights to the potential toxic mechanisms of MC-LR and Phe in aquatic animals.

Topics: Animals; Aquatic Organisms; Daphnia; Drug Interactions; Fresh Water; Inactivation, Metabolic; Life Cycle Stages; Marine Toxins; Microcystins; Phenanthrenes; Water Pollutants, Chemical

Here, Microcystis aeruginosa (M. aeruginosa) was studied to analyze the effects of 0.5 mg L

Topics: Cell Proliferation; Chlorophyll A; Hydrogen-Ion Concentration; Marine Toxins; Microcystins; Microcystis; Naphthalenes; Phenanthrenes

Microcystins and polycyclic aromatic hydrocarbons commonly co-exist in eutrophic freshwater environments. However, their combined toxicity remains unknown. The aim of this study was to evaluate the combined toxic effects of microcystin-LR (MC-LR) and phenanthrene (Phe) on duckweed (Lemna gibba L.) during a short-term exposure (7 d). L. gibba was exposed to a range of environmentally relevant concentrations of MC-LR (5, 50, 250, 500 μg/L) and Phe (0.1, 1, 5, 10 μg/L), both individually and in MC-LR + Phe mixtures (5 + 0.1, 50 + 1, 250 + 5, 500 + 10 μg/L). Subsequently, biomarkers of toxicity such as growth, chlorophyll-a, and antioxidant enzyme activity (catalase, superoxide dismutase, and peroxidase) were analyzed in L. gibba. Growth and the antioxidant system of L. gibba were not significantly inhibited by Phe alone, whereas higher concentrations of individual MC-LR (≥50 μg/L) significantly inhibited growth and induced oxidative stress. Based on Abott's formula, their interaction effects were concentration dependent. Antagonistic effects were observed when exposed to combinations of lower concentrations of MC-LR and Phe (≤50 + 1 μg/L), while additive or synergistic effects were induced at higher concentrations of both compounds (≥250 + 5 μg/L). Moreover, higher concentrations of Phe (≥5 μg/L) increased the accumulation of MC-LR in L. gibba. Our results suggested that the toxic effects of MC-LR and phenanthrene were exacerbated only when they co-exist in water bodies at relatively high concentrations. Consequently, co-existence of MC-LR and Phe at low levels are unlikely to exacerbate ecological hazards to L. gibba in most aquatic environments, at least based on responses of this plant.

Topics: Antioxidants; Araceae; Catalase; Chlorophyll; Drug Synergism; Marine Toxins; Microcystins; Oxidative Stress; Peroxidase; Phenanthrenes; Superoxide Dismutase