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Diuron is a broad-spectrum phenylurea derived herbicide which is commonly used across the globe. Diuron is toxic to the reproductive system of animals and carcinogenic to rat urothelium, and recently found to be genotoxic in human cells. In in vivo , it is metabolized predominately into 3-(3,4-dichlorophenyl)-1-methyl urea (DCPMU) in humans and 3-(3, 4-dichlorophenyl)urea (DCPU) in animals. Information on diuron toxicokinetics and related toxicity in human placenta is absent. We have investigated the toxicokinetics of diuron in ex vivo human placental perfusion and in in vitro human placental microsomes and human trophoblastic cancer cells (BeWo). Diuron crossed human placenta readily in placental perfusion. Furthermore, diuron was metabolized into DCPMU in perfused placenta and in in vitro incubations using microsomes from placentas of smokers. In incubations with placental microsomes from non-smokers, and in BeWo cells, metabolism to DCPMU was detected but only with the highest used diuron concentration (100 μM). Diuron metabolism was inhibited upon addition of α-naphthoflavone, a CYP1A1 inhibitor, underscoring the role of CYP1A1 in the metabolism. In conclusion, it is evident that diuron crosses human placenta and diuron can be metabolized in the placenta to a toxic metabolite via CYP1A1. This implicates in vivo fetal exposure to diuron if pregnant women are exposed to diuron, which may result in fetotoxicity. [ABSTRACT FROM AUTHOR]

Diuron is a herbicide used in agricultural and urban settings and also as an antifouling agent. Recent studies have indicated sublethal responses of diuron in the endocrine system of fish and amphibians. Given the potential of climate change to also alter fish endocrinology, the combination of environmental stressors with diuron may contribute to its sublethal toxicity. In this study, the effects of temperature and salinity on thyroid targets of diuron were assessed in juveniles of the estuarine fish Menidia beryllina under different conditions of salinity (10 and 20‰) and temperature (10 and 20 °C). Environmentally relevant concentrations of diuron affected the growth, and the higher temperature reduced the condition factor of animals. Increased levels of T3 were observed in fish from all treatments, and at 10 °C, T4 levels were augmented at 10‰ but reduced at 20‰. Increased gene expression of deiodinases at 20‰ in both temperatures suggests the influence of salinity on the regulation of hormone imbalance via deiodination pathway activation. Decreased transcripts of thyroid and growth hormone receptors were also observed following diuron treatment. These results indicate that changes in environmental stressors may have significant impacts on the ecological risk of diuron in estuarine fish. [ABSTRACT FROM AUTHOR]

Triazine and urea herbicides are two groups of photosystem II inhibiting herbicides frequently detected in surface, ground and marine waters. Yet, there are few water quality guidelines for herbicides. Ecotoxicity thresholds (ETs) for ametryn, hexazinone and simazine (triazine herbicides) and diuron (a urea herbicide) were calculated using the Australian and New Zealand method for deriving guideline values to protect fresh and marine ecosystems. Four ETs were derived for each chemical and ecosystem that should theoretically protect 99, 95, 90 and 80% of species (i.e. PC99, PC95, PC90 and PC80, respectively). For all four herbicides, the phototrophic species were significantly more sensitive than non-phototrophic species, and therefore, only the former data were used to calculate the ETs. Comparison of the ET values to measured concentrations in 2606 samples from 15 waterways that discharge to the Great Barrier Reef (2011–2015) found three exceedances of the simazine PC99, regular exceedances (up to 30%) of the PC99 in a limited number of rivers for ametryn and hexazinone and frequent (> 40%) exceedances of the PC99 and PC95 ETs in at least four waterways for diuron. There were no exceedances of the marine ETs in inshore reef areas. Further, ecotoxicity data are required for ametryn and hexazinone to fresh and marine phototrophic species, for simazine to marine phototrophic species, for tropical phototrophic species, repeated pulse exposures and long-term (2 to 12 months) exposures to environmentally relevant concentrations. [ABSTRACT FROM AUTHOR]

We examined the effect of two herbicides (Irgarol 1051 and Diuron) on symbiotic dinoflagellates in the hard coral Acropora digitifera using delayed fluorescence (DF), specifically assessing changes in molecular membrane transport, i.e. inflow and outflow rates, and the binding of the herbicides to target proteins in photosystem II. The DF approach is rapid ( e.g. measurement time, 60 s) and non-invasive, and can provide data on the extent of a photosynthetic system and the activity of its electron carriers. The DF of A. digitifera is inhibited 2 h after exposure to 1 μg/L of either Irgarol or Diuron. Analysis of DF inhibition over time by a compartment model suggests that Irgarol exposure results in a relatively higher inflow rate and lower outflow rate than does Diuron exposure. This suggests that Irgarol exposure more strongly inhibits photosynthesis and that the coral symbiotic dinoflagellates recover less from inhibition. [ABSTRACT FROM AUTHOR]

A systematic study on the effects of diuron on the hepatic metabolism was conducted with emphasis on parameters linked to energy metabolism. The experimental system was the isolated perfused rat liver. The results demonstrate that diuron inhibited biosynthesis (gluconeogenesis) and ammonia detoxification, which are dependent of ATP generated within the mitochondria. Conversely, it stimulated glycolysis and fructolysis, which are compensatory phenomena for an inhibited mitochondrial ATP generation. Furthermore, diuron diminished the cellular ATP content under conditions where the mitochondrial respiratory chain was the only source of this compound. Besides the lack of circulating glucose due to gluconeogenesis inhibition, one can expect metabolic acidosis due to excess lactate production, impairment of ammonia detoxification and cell damage due to a deficient maintenance of its homeostasis. Some of the general signs of toxicity that were observed in diuron-treated rats can be attributed, partly at least, to the effects of the herbicide on energy metabolism. [ABSTRACT FROM AUTHOR]

Tests to assess toxic effects on the reproduction of adult C. elegans after 72 h exposure for two chemicals, (3-(3,4-dichlorophenyl)-1,1-dimethylurea (DCMU)), also known as diuron, and silver nanoparticles (Ag NPs) indicated potential, although not significant hormesis. Follow up toxicity tests comparing the potential hormesis concentrations with controls at high replication confirmed that the stimulatory effect was repeatable and also statistically significant within the test. To understand the relevance of the hormesis effects for overall population fitness, full life-cycle toxicity tests were conducted for each chemical. When nematodes were exposed to DCMU over the full life-span, the hormesis effect for reproduction seen in short-term tests was no longer evident. Further at the putative hormesis concentrations, a negative effect of DCMU on time to maturation was also seen. For the Ag NPs, the EC 50 for effects on reproduction in the life-cycle exposure was substantially lower than in the short-term test, the EC 50 s estimated by a three parameter log logistic model being 2.9 mg/L and 0.75 mg/L, respectively. This suggests that the level of toxicity for Ag NPs for C. elegans reproduction is dependant on the life stage exposed and possibly the duration of the exposure. Further, in the longer duration exposures, hormesis effects on reproduction seen in the short-term exposures were no longer apparent. Instead, all concentrations reduced both overall brood size and life-span. These results for both chemicals suggest that the hormesis observed for a single endpoint in short-term exposure may be the result of a temporary reallocation of resources between traits that are not sustained over the full life-time. Such reallocation is consistent with energy budget theories for organisms subject to toxic stress. [ABSTRACT FROM AUTHOR]