Effects of dichlorobenzene on acetylcholine receptors in human neuroblastoma SH-SY5Y cells.

para-Dichlorobenzene (DCB), a deodorant and an industrial chemical, is a highly volatile compound and is known to be an indoor air contaminant. Because of its widespread use and volatility, the toxicity of DCB presents a concern to industrial workers and public. Some toxic aspects of DCB have already been focused but its effects on neuronal signal transduction have been hitherto unknown. The effects of DCB on the cytosolic calcium homeostasis are investigated in human neuroblastoma SH-SY5Y cells in this study. DCB, above 200 microM, was found to induce a rise in cytosolic calcium concentration that could not be counteracted by nicotinic acetylcholine receptor (nAChR) and muscarinic acetylcholine receptor (mAChR) antagonists but was partially inhibited by thapsigargin. To understand the actions of DCB on the acetylcholine receptors, we investigated its effects on the changes of cytosolic calcium concentration following nicotinic AChR stimulation with epibatidine and muscarinic AChR stimulation with methacholine in human neuroblastoma SH-SY5Y cells. DCB inhibited the cytosolic calcium concentration rise induced by epibatidine and methacholine with respective IC(50)s of 34 and 294 microM. The inhibitions of DCB were not the same as thapsigargin's inhibition. In the electrophysiological observations, DCB blocked the influx currents induced by epibatidine. Our findings suggest that DCB interferes with the functional activities of AChR, including its coupling influx currents and cytosolic calcium elevations.

Clear cell and non-clear cell hepatocellular carcinoma: a case report and literature review.

Clear cell hepatocellular carcinoma (HCC) is an uncommon variant of HCC. It is considered to have a better prognosis than non-clear cell HCC, but recent large studies show that there is some controversy. DNA image cytometry reveals diploid and non-diploid DNA content tumors that have different pleomorphisms and mitosis corresponding to different prognoses. Clear cell HCC is classified as focal or diffuse. Herein, we report a rare case of a 61-year-old male with two adjacent hyper- and hypoechoic hepatic nodules and an alpha-fetoprotein concentration of 6,370 ng/mL. Pathologic examination of a specimen obtained during wedge hepatectomy showed both clear cell and non-clear cell HCC. Bone metastasis was later found. We suggest that a patient with clear cell HCC should be followed up closely after complete resection.

Comparative suppression of phthalate monoesters and phthalate diesters on calcium signalling coupled to nicotinic acetylcholine receptors.

Phthalates, such as butyl benzyl phthalate (BBP), di-n-butyl phthalate (DBP), and their metabolites (mono-buyl phthalate [MBP], mono-benzyl phthalate [MBzP] and phthalic acid [PA]), are known to obstruct normal development in mammals. BBP and DBP have been reported to have estrogenic activity, while MBP and MBzP exhibit weak or no estrogenic effects. We previously showed that BBP and DBP have inhibitory roles on nicotinic acetylcholine receptors. Nicotinic acetylcholine receptors are widely distributed and have roles in developmental processes. In this study, the effects of BBP, DBP, MBP, MBzP and PA on calcium signaling coupled to nicotinic acetylcholine receptors was investigated in bovine adrenal chromaffin cells and human neuroblastoma SH-SY5Y cells. Following an epibatidine-induced [Ca2+](c) increase, the IC(50)s of BBP, DBP, MBzP and MBP were 3.41, 5.01, 432 and 695 microM in bovine adrenal chromaffin cells and 0.28, 0.44, 58 and 116 microM in human SH-SY5Y cells, respectively. Although PA suppressed the epibatidine-induced [Ca2+](c) increase, the suppression was less than with MBP. The suppression potency of phthalates was related to their chemical structures. The suppression effects of BBP, DBP, MBP and MBzP remained similar potency under chronic treatments. This study demonstrated that MBP, MBzP and PA, the metabolites of BBP and DBP, had suppressor roles on the calcium signaling pathway coupled to nicotinic receptors.