Nitrate and sodium nitroprusside alter the development of Asian black-spined toads' embryos by inducing nitric oxide production.

Nitrate is the most stable and abundant form of inorganic nitrogen in water. However, owing to human activities, the nitrate concentration in aquatic ecosystems has notably increased worldwide. One of the mechanisms underlying nitrate toxicity in vertebrates includes the functional inhibition of the sodium iodide symporter, resulting in thyroid dysfunction. In this study, we aimed to determine the alternative mechanisms underlying the toxicological effects of nitrates on the Asian black-spined toad (Duttaphrynus melanostictus). Embryos of D. melanostictus were exposed to sodium nitroprusside (SNP, positive control) or 100 mg/L nitrate-nitrogen (NO3-N) for 184 h. We observed that both SNP and NO3-N significantly decreased body mass and length and delayed developmental processes. Teratogenic symptoms, including tumors, hyperplasia, and abdominal edema, were also observed in embryos exposed to SNP and NO3-N. Furthermore, SNP and NO3-N significantly increased nitric oxide levels in the embryos, altering the thyroid hormone, nitrogen, cytochrome P450-mediated drug, and xenobiotic metabolism signaling pathways, as well as the pathway involved in chemical carcinogenesis. The similar toxicological effects of SNP and NO3-N suggested that nitrate toxicity resulted from the generation of nitric oxide. Therefore, the present study provides insights into an alternative mechanism underpinning nitrate toxicity, which is useful for the conservation of amphibians in nitrate-rich environments.

A strigolactone signal is required for adventitious root formation in rice.

BACKGROUND AND AIMS: Strigolactones (SLs) and their derivatives are plant hormones that have recently been identified as regulating root development. This study examines whether SLs play a role in mediating production of adventious roots (ARs) in rice (Oryza sativa), and also investigates possible interactions between SLs and auxin. METHODS: Wild-type (WT), SL-deficient (d10) and SL-insensitive (d3) rice mutants were used to investigate AR development in an auxin-distribution experiment that considered DR5::GUS activity, [(3)H] indole-3-acetic acid (IAA) transport, and associated expression of auxin transporter genes. The effects of exogenous application of GR24 (a synthetic SL analogue), NAA (α-naphthylacetic acid, exogenous auxin) and NPA (N-1-naphthylphalamic acid, a polar auxin transport inhibitor) on rice AR development in seedlings were investigated. KEY RESULTS: The rice d mutants with impaired SL biosynthesis and signalling exhibited reduced AR production compared with the WT. Application of GR24 increased the number of ARs and average AR number per tiller in d10, but not in d3. These results indicate that rice AR production is positively regulated by SLs. Higher endogenous IAA concentration, stronger expression of DR5::GUS and higher [(3)H] IAA activity were found in the d mutants. Exogenous GR24 application decreased the expression of DR5::GUS, probably indicating that SLs modulate AR formation by inhibiting polar auxin transport. The WT and the d10 and d3 mutants had similar expression of DR5::GUS regardless of exogenous application of NAA or NPA; however, AR number was greater in the WT than in the d mutants. CONCLUSIONS: The results suggest that AR formation is positively regulated by SLs via the D3 response pathway. The positive effect of NAA application and the opposite effect of NPA application on AR number of WT plants also suggests the importance of auxin for AR formation, but the interaction between auxin and SLs is complex.