Reproductive toxicity of enrofloxacin in Caenorhabditis elegans involves oxidative stress-induced cell apoptosis

Fluoroquinolone antibiotics(FQs)that persist and bioaccumulate in the environment have aroused people’s great concern.Here,we studied the adverse effects of FQs in soil animals of Caenorhabditis elegans via food-chronically exposure.The result shows C.elegans exposed to FQs exhibited reproductive toxicity with small-brood size and low-egg hatchability.To study the underlying mechanism,we conduct a deep investigation of enrofloxacin(ENR),one of the most frequently detected FQs,on nematodes which is one of commonly used animal indicator of soil sustainability.The concentration-effect curves simulated by the Hill model showed that the half effect concentrations(EC50)of ENR were(494.3±272.9)μmol/kg and(107.4±30.9)μmol/kg for the brood size and the hatchability,respectively.Differential gene expression between the control and the ENR-exposure group enriched with the oxidative stress and cell apoptosis pathways.The results together with the enzyme activity in oxidative stress and the cell corpses suggested that ENR-induced reproductive toxicity was related to germ cell apoptosis under oxidative stress.The risk quotients of some soil and livestock samples were calculated based on the threshold value of EC10 for the egg hatchability(2.65μmol/kg).The results indicated that there was possible reproductive toxicity on the nematodes in certain agricultural soils for the FQs.This study suggested that chronic exposure to FQs at certain levels in environment would induce reproductive toxicity to the nematodes and might reduce the soil sustainability,alarming the environment risks of antibiotics abuse.

Immunohistopathology of the contralateral testis of rats undergoing experimental torsion of the spermatic cord

Aim： To evaluate the immunohistopathological changes in the contralateral testis of rats after an experimental spermatic cord torsion. Methods： Male Sprague-Dawley rats of 45-50 days old were subjected to a 720° unilateral spermatic cord torsion for 10, 30 and 80 days （experimental group, E）, respectively or sham operation （control group, C）. Histopathology of the contralateral testis as well as germ cell apoptosis were studied using the Terminal Deoxynucleotidyl Transferase Biotin-dUTP Nick End Labeling （TUNEL） technique. The number of testicular lymphocytes, mast cells and macrophages, and the expression of tumor necrosis factor-α （TNF-α） and its receptor （TNFR1） in testicular cells of the contralateral testis were quantified by histochemistry and immunohistochemistry. TNF-α concentration in testicular fluid was determined by ELISA. Results： In the contralateral testis of rats from the E group, the maximal degree of damage of the germinal epithelium was seen 30 days after torsion. At this time we observed in the E group vs. the C group increases： （i） the number of testicular T-lymphocytes; （ii） the number of testicular mast cells and macrophages; （iii） the percentage of macrophages expressing TNF-α; （iv） TNF-α concentration in testicular fluid; （v） the number of apoptotic germ cells; and （vi） the number of TNFR1^＋ germ cells. Conclusion： Experimental spermatic cord torsion induces, in the contralateral testis, a focal damage of seminiferous tubules characterized by apoptosis and sloughing of germ cells. Results suggest humoral and cellular immune mediated testicular cell damage in which macrophages and mast cells seem to be involved in the induction of germ cell apoptosis through the TNF-α/TNFR1 system and in the modulation of the inflammatory process.