Search

Objective To examine the role of Cd-induced reactive oxygen species (ROS) generation in the apoptosis of neuronal cells. Methods Neuronal cells (primary rat cerebral cortical neurons and PC12 cells) were incubated with or without Cd post-pretreatment with rapamycin (Rap) or N-acetyl- l -cysteine (NAC). Cell viability was determined by MTT assay, apoptosis was examined using flow cytometry and fluorescence microscopy, and the activation of phosphoinositide 3′-kinase/protein kinase B (Akt)/mammalian target of rapamycin (mTOR) and mitochondrial apoptotic pathways were measured by western blotting or immunofluorescence assays. Results Cd-induced activation of Akt/mTOR signaling, including Akt, mTOR, p70 S6 kinase (p70 S6K), and eukaryotic initiation factor 4E binding protein 1 (4E-BP1). Rap, an mTOR inhibitor and NAC, a ROS scavenger, blocked Cd-induced activation of Akt/mTOR signaling and apoptosis of neuronal cells. Furthermore, NAC blocked the decrease of B-cell lymphoma 2/Bcl-2 associated X protein (Bcl-2/Bax) ratio, release of cytochrome c, cleavage of caspase-3 and poly(ADP-ribose) polymerase (PARP), and nuclear translocation of apoptosis-inducing factor (AIF) and endonuclease G (Endo G). Conclusion Cd-induced ROS generation activates Akt/mTOR and mitochondrial pathways, leading to apoptosis of neuronal cells. Our findings suggest that mTOR inhibitors or antioxidants have potential for preventing Cd-induced neurodegenerative diseases. [ABSTRACT FROM AUTHOR]

The article offers information on a study which examines the effects of zearalenone on expression and apoptosis of caspase 3 and 9 in Leydig cells.

The article discusses the study which investigates the effect of trichlorfon on the nerve cells of rat cortical neuron.

The article presents a study which examines the impacts of trichlorfon in cortical neurons of rat. The study exposes Sprague-Dawley rats cell culture at different durations and concentrations of trichlorfon and measures its effect on apoptosis rate, adenosine triphosphate (ATP) activity, and mitochondrial membrane potential. Result shows that 12 hours exposure leads to increased apoptosis and declined mitochondrial membrane potential and ATPase activity.

The article presents a study on the determination of serum concentrations of trace elements including selenium, zinc and iron at different physiological stages of dairy cows. It also highlights the oxidative status of serum in dairy cows which are not related to age. It states that the serum concentrations of the trace elements and the oxidative status of serum in were the lowest which indicate imbalances in one month before calving and lactation.

The article reports on the study of the influence of 1α, 25-dihydroxyvitamin D3 on the cell cycle and proliferation of osteoblasts. Isolated osteoblasts from skull were dealt with different concentrations of 1α, 25-dihydroxyvitamin D3. Results show that low doses of 1α, 25-dihydroxyvitamin D3 can improve proliferation and inhibit differentiation while high doses do the opposite.

The article presents a study which examines the effect of calcium on proliferation and differentiation as well as cell cycle of osteoblasts in rats.

The article presents a study which determines the influence of osteoprotegerin (OPG) and receptor activator NF-kB ligand (RANKL) on duck's osteoclasts formation and activation. The result showed that the area of lacunar resorption decreased with concentration and increasing of OPG-RANKL may advance osteoclasts (OC) formation and activation. On the other hand, OPG may limit bone absorbing activity through inhibiting the formation and activation of OC.

The article discusses a study on the primary culture and identification of renal tubular epithelial cells in Sprague Dawley (SD) rat by using several methods, such as mechanical grinding, immunohistochemical method, and cytochemical staining.

The article presents a study regarding the toxicological effects of the two heavy metals including lead acetate and cadmium chloride towards the kidneys of rats. It investigates the antioxidant indices and ultrastructural findings in the renal cortex. It states that oxidative damage is one of the synergestic effect of lead and cadmium coadministration which results to nephrotoxicity.

A high concentration of Zearalenone (ZEA) will perturb the differentiation of germ cells, and induce a death of germ cells, but the toxic mechanism and molecular mechanism remain unclear. The Sertoli cells (SCs) play an irreplaceable role in spermatogenesis. In order to explore the potential mechanism of ZEA male reproductive toxicity, we studied the effects of ZEA on cell proliferation, cell-cycle distribution, cell-cycle-related proteins and autophagy-related pathway the PI3K/Akt/mTOR signaling in primary cultured rats SCs, and the effects of autophagy and PI3K/AKT/m TOR signaling pathway on the SCs cell-cycle arrest induced by ZEA treated with the autophagy promoter RAPA, autophagy inhibitor CQ, and the PI3K inhibitor LY294002, respectively. The data revealed that ZEA could inhibit the proliferation of SCs by arresting the cell cycle in the G2/M phase and trigger the autophagy via inhibiting the PI3K/Akt/m TOR signaling pathway. Promoting or inhibiting the level of autophagy could either augment or reverse the arrest of cell cycle. And it was regulated by PI3K/Akt/m TOR signaling pathway. Taken together, this study provides evidence that autophagy and PI3K/Akt/m TOR signaling pathway are involved in regulating rats primary SCs cell-cycle arrest due to ZEA in vitro. To some extent, ZEA-induced autophagy plays a protective role in this process. [ABSTRACT FROM AUTHOR]

Avian bone metabolism diseases affect the development and production of chickens, and many of these diseases can be prevented and controlled by balanced nutrition and hormone medicine. The steroid hormone 1α,25-dihydroxyvitamin D 3 plays a key role in maintaining the balance of avian bone metabolism. Clinically, 1α,25-(OH) 2 D 3 has been used to treat several bone diseases. Although several previous studies have investigated the effects of 1α,25-(OH) 2 D 3 on osteoclastogenesis, the mechanisms underpinning osteoclast (OC) activity remain largely unknown. Herein, we used molecular and cell biology approaches to demonstrate that 1α,25-(OH) 2 D 3 increases avian OC formation and activity, and upregulates bone resorption-related genes. Moreover, 1α,25-(OH) 2 D 3 regulates the OC cytoskeleton by increasing the formation of zipper-like structure in OC precursor cells to potentiate OC activity via the Src/Rac1 signaling pathway. These findings provide new insight into the role of 1α,25-(OH) 2 D 3 in OC activity., (Copyright © 2018 Elsevier Inc. All rights reserved.)

The steroid hormone 1α,25-dihydroxyvitamin D 3 [1α,25-(OH) 2 D 3 ] plays an important role in maintaining a balance in calcium and bone metabolism. To study the effects of 1α,25-(OH) 2 D 3 on osteoclast (OC) formation and bone resorption, OC differentiation was induced in bone marrow-derived mononuclear cells from Wistar rats with the addition of macrophage colony stimulating factor and receptor activator for nuclear factor-κB ligand in vitro . Cells were then treated with 1α,25-(OH) 2 D 3 at 10 -9 , 10 -8 or 10 -7 mol/l. OCs were identified using tartrate-resistant acid phosphatase staining and activity was monitored in the absorption lacunae by scanning electron microscopy. Expression levels of functional proteins associated with bone absorption, namely carbonic anhydrase II, cathepsin K and matrix metalloproteinase-9 were evaluated by western blot analysis. The results showed that 1α,25-(OH) 2 D 3 inhibited the formation and activation of OCs in a dose-dependent manner and downregulated the expression levels of bone absorption-associated proteins.

To investigate 1α,25-(OH)₂D₃ regulation of matrix metalloproteinase-9 (MMP-9) protein expression during osteoclast formation and differentiation, receptor activator of nuclear factor kB ligand (RANKL) and macrophage colony-stimulating factor (M-CSF) were administered to induce the differentiation of RAW264.7 cells into osteoclasts. The cells were incubated with different concentrations of 1α,25-(OH)₂D₃ during culturing, and cell proliferation was measured using the methylthiazol tetrazolium method. Osteoclast formation was confirmed using tartrate-resistant acid phosphatase (TRAP) staining and assessing bone lacunar resorption. MMP-9 protein expression levels were measured with Western blotting. We showed that 1α,25-(OH)₂D₃ inhibited RAW264.7 cell proliferation induced by RANKL and M-CSF, increased the numbers of TRAP-positive osteoclasts and their nuclei, enhanced osteoclast bone resorption, and promoted MMP-9 protein expression in a concentration-dependent manner. These findings indicate that 1α,25-(OH)₂D₃ administered at a physiological relevant concentration promoted osteoclast formation and could regulate osteoclast bone metabolism by increasing MMP-9 protein expression during osteoclast differentiation.