Effects on Bioaccumulation, Growth Performance, Hematological Parameters, Plasma Components, and Antioxidant Responses in Starry Flounder (Platichthys stellatus) Exposed to Dietary Cadmium and Ascorbic Acid.

This study evaluates the toxic effects of dietary Cd and mitigative effects of AsA supplementation by measuring the growth performance, bioaccumulation, hematological parameters, plasma components, and antioxidant responses of Starry flounder (Platichthys stellatus). Platichthys stellatus (mean weight, 69.5 ± 1.4 g; mean length, 18.2 ± 0.21 cm) was fed with dietary cadmium-ascorbic acid (Cd-AsA) composed of C0A0, C0A500, C0A1000, C40A0, C40A500, C40A1000, C80A0, C80A500, and C80A1000 mg of Cd-AsA per kg diet for four weeks. Our results showed that Cd accumulation significantly increased in proportion to the Cd concentration, where the highest levels were observed in the intestine, followed by the kidney, liver, and gills. Dietary AsA significantly mitigated the Cd accumulation in all tissues, and the reduction in Cd accumulation was proportional to the increase in AsA concentration. Dietary Cd has adverse effects on growth performance (body weight gain, specific growth rate, feed conversion ratio, and hepatosomatic index) and can alter the hematological parameters (red blood cell count, hematocrit, and hemoglobin), plasma components (glucose, total protein, glutamic oxaloacetic transaminase, and glutamic pyruvic transaminase), and antioxidant responses (superoxide dismutase, catalase, glutathione S-transferase, and glutathione). Dietary AsA restored the decreased growth performance parameters and the altered hematological parameters, plasma components, and antioxidant responses caused by the dietary Cd exposure. The results of this study showed that dietary Cd is toxic to P. stellatus, while dietary AsA is effective in mitigating the toxic effects of Cd.

Neuroprotective effects of the new diterpene, CBNU06 against beta-amyloid-induced toxicity through the inhibition of NF-kappaB signaling pathway in PC12 cells.

Alzheimer's disease is the most common form of dementia, causing progressive cognitive dysfunction, particularly memory loss. Recently, modulation of beta-amyloid (Abeta) toxicity, one of the major potential causes of Alzheimer's disease, has emerged as a possible therapeutic approach to control the onset of Alzheimer's disease. In this study, we investigated the neuroprotective effects and possible mechanisms by which 19-hydroxy-1alpha,6-diacetoxy-6,7-seco-ent-kaur-16-en-15-one-7,20-olide (named as CBNU06), a new diterpene isolated from Isodon japonicus, acts against Abeta-induced toxicity in PC12 cells. Pretreatment with CBNU06 (20 microg/ml) prior to Abeta(25)(-35) (25 microM) significantly increased the viability of PC12 cells in a dose-dependent manner when examined by Hoechst staining, MTT assay and Trypan blue exclusion assay. This protective effect was accompanied by the decrease in translocation of NF-kappaB p50 and p65 from the cytoplasm to the nucleus, and followed by the decrease in cyclooxygenase-2 (COX-2) levels. In addition, pretreatment with CBNU06 significantly reversed the effect of Abeta on Bax and Bcl-2. Taken together, these results suggest that CBNU06 protected PC12 cells against Abeta-induced neurotoxicity through the inhibition of the NF-kappaB signaling pathways. Therefore, CBNU06 has the possible beneficial effects in Alzheimer's disease by attenuating Abeta-induced toxicity.