Hepatotoxicity induced in rats by chronic exposure to F-53B, an emerging replacement of perfluorooctane sulfonate (PFOS).

A plethora of studies have shown the prominent hepatotoxicity caused by perfluorooctane sulfonate (PFOS), yet the research on the causality of F-53 B (an alternative for PFOS) exposure and liver toxicity, especially in mammals, is largely limited. To investigate the effects that chronic exposure to F-53 B exert on livers, in the present study, male SD rats were administrated with F-53 B in a certain dose range (0, 1, 10, 100, 1000 μg/L, eight rats per group) for 6 months via drinking water and the hepatotoxicity resulted in was explored. We reported that chronic exposure to 100 and 1000 μg/L F-53 B induced remarkable histopathological changes in liver tissues such as distinct swollen cells and portal vein congestion.

Repeated radon exposure induced epithelial-mesenchymal transition-like transformation via disruption of p53-dependent mitochondrial function.

Backgrouds: As a human carcinogen, radon and its progeny are the second most important risk factor for lung cancer after smoking. The tumor suppressor gene, , is reported to play an important role in the maintenance of mitochondrial function. In this work, we investigated the association between p53 and p53-responsive signaling pathways and radon-induced carcinogenesis.

Protection of melatonin against long-term radon exposure-caused lung injury.

Radon is one of the major pathogenic factors worldwide. Recently, epidemiological studies have suggested that radon exposure plays an important role in lung injury, which could further cause cancer. However, the toxic effects and underlying mechanism on lung injury are still not clear.

SQR mediates therapeutic effects of HS by targeting mitochondrial electron transport to induce mitochondrial uncoupling.

Hydrogen sulfide (HS) is a gasotransmitter and a potential therapeutic agent. However, molecular targets relevant to its therapeutic actions remain enigmatic. Sulfide-quinone oxidoreductase (SQR) irreversibly oxidizes HS.

Nonylphenol induces pancreatic damage in rats through mitochondrial dysfunction and oxidative stress.

The organic alkylphenol 4-nonylphenol (NP) is regarded to be an endocrine disrupting chemical (EDC), one of the widely diffused and stable environmental contaminants. Due to its hydrophobicity and long half-life, NP can easily accumulate in living organisms, including humans, where it displays a series of toxic effects. It has been widely reported that NP affects male reproduction.

Cytogenetic evaluation for the genotoxicity of bisphenol-A in Chinese hamster ovary cells.

Bisphenol A (BPA), identified as an endocrine disruptor, is an important man-made compound used in a wide range of consumer products. The MTT assay, comet assay, micronucleus test, chromosome aberration test, and Ames assay were conducted to assess the cytotoxic, genotoxic, cytogenetic effects, and mutagenic activity of BPA. After BPA exposure, we showed significant increases in cytotoxicity and level of DNA damage indicated by Olive tail moment, tail length, and % tail DNA in a similar dose- and time-dependent manner.

Pharmacokinetics, tissue distribution, and metabolites of a polyvinylpyrrolidone-coated norcantharidin chitosan nanoparticle formulation in rats and mice, using LC-MS/MS.

A novel formulation containing polyvinylpyrrolidone (PVP) K(30)-coated norcantharidin (NCTD) chitosan nanoparticles (PVP-NCTD-NPs) was prepared by ionic gelation between chitosan and sodium tripolyphosphate. The average particle size of the PVP-NCTD-NPs produced was 140.03 ± 6.

[Molecular mechanism of radiosensitizing effect of paclitaxel].

Background & Objective: Paclitaxel is a radiosensitizer which may stabilize microtubules, block the G2/M phase of the cell cycle and thus modulate the radioresponsiveness of tumor cells. However, its potential molecular mechanisms of radiosensitization have not been well understood yet. This study was to investigate the radiosensitizing effect of paclitaxel on human oral epithelium carcinoma (KB) cell line and to explore the molecular mechanism of radiosensitization.

Effect of Nd3+ ion on carboxylation activity of ribulose-1,5-bisphosphate carboxylase/oxygenase of spinach.

Neodymium (Nd), as a member of rare earth elements, proved to enhance the photosynthesis rate and organic substance accumulation of spinach through the increase in carboxylation activity of Rubisco. Although the oxygenase activity of spinach Rubisco was slightly changed with the Nd(3+) treatment, the specific factor of Rubisco was greatly increased. It was partially due to the promotion of Rubisco activase (R-A) activity but mainly to the formation of Rubisco-Rubisco activase super-complex, a heavier molecular mass protein (about 1200kD) comprising both Rubisco and Rubisco activase.