Autophagy Attenuates MnCl2-induced Apoptosis in Human Bronchial Epithelial Cells.

Objective: To investigate the role of autophagy in MnCl2-induced apoptosis in human bronchial epithelial 16HBE cells.

Methods: Cell proliferation was measured by MTT assay. Mitochondrial membrane potential (MMP) and apoptosis were measured by flow cytometry.

PINK1/Parkin-mediated mitophagy play a protective role in manganese induced apoptosis in SH-SY5Y cells.

Manganese (Mn) as an environmental risk factor of Parkinson's disease (PD) is considered to cause manganism. Mitophagy is thought to play a key role in elimination the injured mitochondria. The goal of this paper was to explore whether the PINK1/Parkin-mediated mitophagy is activated and its role in Mn-induced mitochondrial dysfunction and cell death in SH-SY5Y cells.

S phase cell percentage normalized BrdU incorporation rate, a new parameter for determining S arrest.

In this study, a new parameter, S phase cell percentage (S fraction) normalized BrdU (SFN-BrdU) incorporation rate, was introduced to detect S arrest. The results showed a positive linear correlation between the BrdU incorporation rate and the S fraction in unperturbed 16HBE cells. Theoretical analysis indicated that only S arrest could result in a decrease in the SFN-BrdU incorporation rate.

Down-regulation of mitotic checkpoint in transformed human embryo lung fibroblasts induced by N-methyl-N'-nitro-N-nitrosoguaridine.

Background: Mutations in mitotic checkpoint genes have been detected in several human cancers, which exhibit chromosome instability. We wanted to know whether mutation of hBub1 could occur in transformed human embryo lung fibroblasts (HELF) cells induced by a chemical carcinogen.

Methods: HELF cells were transformed by N-methyl-N'-nitro-N-nitrosoguaridine (MNNG), and three flasks of transformed HELF cells (named as T1, T2, and T3) were selected as amplifiers, and mutations of hBub1 in these transformed cells were analyzed by PCR-SSCP and sequencing.

Cadmium directly induced the opening of membrane permeability pore of mitochondria which possibly involved in cadmium-triggered apoptosis.

The mitochondrial damage induced by cadmium has been well established, but its mechanism and its relationship with cadmium-induced apoptosis are elusive until now. Our research showed that cadmium could directly lead to the dysfunction of isolated mitochondria from mouse liver, including the inhibition of respiration, the opening of permeability transition pore (PTP), the loss of transmembrane potential, and the release of cytochrome c. These mitochondrial changes were completely suppressed by Bcl-xL and Ruthenium Red (RR).

The inhibitory effects of manganese on steroidogenesis in rat primary Leydig cells by disrupting steroidogenic acute regulatory (StAR) protein expression.

Manganese is known to impede the male reproductive function, however, the mechanisms through which the adverse effects are mediated are not clearly elucidated. In order to get insight into those mechanisms, the effects of manganese on the biosynthesis of testosterone by primary rat Leydig cells were examined. Primary Leydig cells were exposed to various concentrations of manganese chloride for different periods of time.

The role of thiol reduction in hydroquinone-induced apoptosis in HEK293 cells.

Hydroquinone (HQ) is a chemical used as a reducing agent, antioxidant, polymerization inhibitor, and chemical intermediate. It has a minor use as a bleaching agent in dermatologic preparations. HQ also occurs as a main metabolite of benzene.