Exposure to pyrazosulfuron-ethyl induces immunotoxicity and behavioral abnormalities in zebrafish embryos.

Pyrazosulfuron-ethyl is one of the most widely used herbicides in agriculture and can be widely detected in aquatic ecosystems. However, its biosafety, including its potential toxic effects on aquatic organisms and its mechanism, is still poorly understood. As an ideal vertebrate model, zebrafish, the effect of pyrazosulfuron-ethyl on early embryonic development and immunotoxicity of zebrafish can be well evaluated. From 10 to 72 h post fertilization (hpf), zebrafish embryos were exposed to 1, 5, and 9 mg/L pyrazosulfuron-ethyl which led in a substantial reduction in survival, total length, and heart rate, as well as a range of behavioral impairments. In zebrafish larvae, the number of neutrophils and macrophages was considerably decreased and oxidative stress levels increased in a dose-dependent way after pyrazosulfuron-ethyl exposure. And the expression of immune-related genes, such as TLR-4, MyD88 and IL-1ß, were downregulated by pyrazosulfuron-ethyl exposure. Moreover, pyrazosulfuron-ethyl exposure also inhibited motor behavior. Notch signaling was upregulated after exposure to pyrazosulfuron-ethyl, while inhibition of Notch signaling pathway could rescue immunotoxicity. Therefore, our findings suggest that pyrazosulfuron-ethyl has the potential to induce immunotoxicity and neurobehavioral changes in zebrafish larvae.

The hepatocyte in the innate immunity.

The hepatocytes, as the main cells in the liver, exert liver functions by expressing innate immune receptors. The innate immune receptors include Toll-like receptors (TLRs), RIG-like receptors (retinoic acid inducible gene I-like receptors, RLRs) and NOD-like receptors (nucleotide binding oligomerization domain-like receptors, NLRs). The hepatocytes, recognize extracellular pathogen-associated molecular patterns (PAMPs) and intracellular damage-associated molecular patterns (DAMPs) through the above receptors. After the activation of the innate immune receptors, the hepatocytes produce cytokines, such as interferon (IFN), to protect the liver, through a series of signaling cascades.

California almond shelf life: lipid deterioration during storage.

UNLABELLED: The effects of storage conditions on the lipid deterioration in California almond nuts and sliced were studied. Natural whole almonds with or without polyethylene (PE) packaging and blanched whole almonds and sliced with PE packaging were stored in 10 different storage conditions which were combinations of different temperatures and relative humidity levels. The peroxide values (PVs), iodine values (IVs), and free fatty acids (FFAs) were monitored during the storage. The PVs in the natural samples did not change noticeably whereas the blanched samples changed greatly, indicating that skins may have played a significant role. The IVs decreased slightly in the 1st 150 d of storage and then leveled off. The slightly faster changes in IVs in the blanched samples coincided with the greater changes in PVs in the blanched samples. The natural samples exhibited much higher FFA levels than the blanched samples after storage. In general, FFA increased with increasing storage time, temperature, and humidity. Highest levels of FFA were observed in the samples stored at high temperature and high humidity. PRACTICAL APPLICATION: The results reported in this article provide useful information that almond producers and processors could use to develop their storage and transport processes.