The aim of this study was to investigate the effects of Portulaca oleracea extracts on growth performance and microbial populations in the ceca of broilers. A total of 120 one-day-old broilers were randomly divided into 3 groups. Portulaca oleracea extracts were added to diets at 0.2 and 0.4% (wt/wt; POL-0.2, POL-0.4), respectively. The control (CON) group was administered with no P. oleracea extract supplementation. Body weight gain and feed conversion ratio were recorded every 2 wk. On d 28 and 42, the cecal contents were collected and assayed for Escherichia coli, Lactobacillus, and Bifidobacterium populations. Additionally, the pH of the ileum and cecum was measured. The results showed that both on d 28 and 42 BW gain of P. oleracea extract supplementation groups was significantly higher, whereas the feed conversion ratio was lower (P< 0.05) compared with CON. On d 28 and 42, significantly (P < 0.05) fewer E. coli were recovered from ceca of broilers provided with the POL-0.2 diet than from broilers provided with the control diet. The quantities of Lactobacillus and Bifidobacterium of POL-0.2 were significantly (P < 0.05) higher than CON. Results showed P. oleracea extracts have no distinct influence on intestinal pH. These data suggest that P. oleracea extract supplementation significantly altered the cecal bacterial community without affecting the intestinal pH.

Cadmium, a heavy metal, is a toxic environmental and industrial pollutant. Exposure to cadmium can lead to the toxic effects in a variety of tissues, also including the brain. The present study investigated the effect of cadmium exposure on the histopathology of cerebral cortex in juvenile mice. Juvenile mice were randomly divided into control, low (1.87 mg/kg), medium (3.74 mg/kg), and high (7.48 mg/kg) dose groups. After cadmium exposure by drinking water for 10 days, the cerebral cortex was obtained for histopathology studies. The medium and high dose of cadmium, rather than low dose, could induce the histopathology alterations of cerebral cortex in a dose-dependent manner. In the high-dose group, microstructure significantly showed pia mater encephali divorcing from cerebral cortex layer, serious hyperemia of blood capillary in pia mater encephali and cerebral cortex, broadening vessel peripheral clearance, a large number of eosinophil leukocyte infiltrating around blood vessel, vacuolar degeneration in part granule cells, and obviously increasing apoptotic cells. Ultrastructure obviously displayed marginalized heterochromatin, incomplete or fused nuclear membranes, broadened perinuclear space, ambiguous mitochondria cristae, decreased synaptic cleft, and fused presynaptic and postsynaptic membrane. Our results revealed that cadmium at the middle and high dose could induce obvious microstructure and ultrastructure alterations of cerebral cortex in juvenile mice, which may be one important mechanism of cadmium neurotoxicity.

The aim of this study was to investigate microstructure and ultrastructure alterations in the pallium of immature mice exposed to cadmium. Forty immature mice were randomly divided into control, 1/100 LD (1.87 mg/kg, low), 1/50 LD (3.74 mg/kg, medium), and 1/25 LD (7.48 mg/kg, high) dose groups. After oral cadmium exposure for 40 days, the pallium of mice was obtained for microstructure and ultrastructure studies. The results showed that both microstructure and ultrastructure alterations of the pallium were observed in all treated mice and the most obvious alterations were in the high dose group. Microstructural analysis showed seriously congested capillary in the pia mater of the pallium in the high cadmium group. Meanwhile, vacuolar degenerate or karyopyknosis presented in some neurocytes, capillary quantity, and the number of apoptotic cells increased, some neurocytes became hypertrophy, the pia mater separated from the cortex, and local hemorrhage and accompanied inflammatory cell infiltration were also observed. Ultrastructural analysis showed that rough endoplasmic reticulum was expanded, heterochromatin marginalized, perinuclear space distinctly broadened, swelling and vacuolization mitochondria appeared, synapse was swelling, presynaptic and postsynaptic membranes presented fusion, and most of mitochondrial cristae were ambiguous. The results indicated that cadmium exposure for 40 days induced dose-dependent microstructure and ultrastructure alterations in pallium of immature mice.

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