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The purpose of this research was to determine mitochondrial and lysosomal damage and oxidative stress status in blood lymphocytes of lead-zinc miners. This research was performed in 10 mine workers who have been in contact with lead and zinc in comparison to a control group containing 10 healthy volunteers. Lymphocytes were isolated from peripheral blood using the Ficoll standard method and then mitochondrial and lysosomal damage and oxidative stress were evaluated. The level of reactive oxygen species (ROS), collapse in the mitochondrial membrane potential (MMP) collapse, and glutathione disulfide (GSSG) content, and lysosomal damage in miners were higher than the control group. Also, viability and glutathione (GSH) content were decreased. The lymphocytes of workers of a lead-zinc mine are more susceptible to oxidative stress, mitochondrial and lysosomal damage. The proper use of safety equipment can reduce the risk of toxic agents and their subsequent hazards for mine workers.

Lithium (Li) is a widely-used medication for the treatment of patients with bipolar disorder. Li causes different complications. One of the most important adverse effects of Li is neurotoxicity. Neurotoxicity is usually irreversible which may lead to very important complications. The symptoms of Li-induced neurotoxicity include tremor, delirium, seizures, coma, and death. In this study, we wanted to evaluate the exact sub-cellular mechanisms of Li-induced neurotoxicity.

Arsenic (As) is a semi-metal which causes health problems in human, and immune system has been documented as one of the main target of arsenic toxicity. Apoptosis has a crucial role in regulation of immune system, but it can also have an important role in As immune suppression. So, we decided to assess the comprehensive mechanism of As cytotoxic effect on lymphocytes isolated from human blood. We determine the direct effect of arsenic on human lymphocytes which have a key role in immune system functionality. To evaluate the mechanism of arsenic toxicity on human lymphocytes, we use accelerated cytotoxicity mechanisms screening (ACMS) technique. Lymphocytes were isolated from blood of healthy persons using Ficoll-paque PLUS standard method. Following treatment of human lymphocytes with 0.05-50 μM of arsenic for 12 h, cell viability was measured. For determination of mechanistic parameters, isolated human lymphocytes incubated with 1/2IC5012h (7.5 μM), IC5012h (15 μM) and 2IC5012h (30 μM) for 2, 4 and 6 h. The results of this study demonstrate arsenic-associated apoptosis in human lymphocytes is mainly through enhancement of intracellular calcium which causes oxidative stress and following adverse effect on lymphocytes organelles (like mitochondria and lysosome). Involvement of cellular proteolysis, activation of caspase-3, lipid peroxidation and stimulation of cytokines (IL2, INF-gamma and TNF-alpha) production were also associated with arsenic induced lymphocyte toxicity.

Lead (Pb) is one of the most important heavy metals that possess many applications in different kinds of industrial procedures and consumer products. The adverse effects of Pb on different parts of the immune system have been reported in various studies. Although it has been shown that high concentrations of Pb have low cytotoxicity on human lymphocytes, the effects of non-cytotoxic concentrations of Pb (detected in human blood) on cellular organelles and oxidative stress factors of human lymphocytes have yet to be determined. In this study, human lymphocytes were obtained from the blood of healthy male volunteers through the use of the Ficoll standard method. The intention of this paper was to determine the effects of non-cytotoxic concentrations of Pb on human lymphocytes using the accelerated cytotoxicity mechanism screening technique. For determination of cell viability, lymphocytes were treated with 0–1 mm Pb for 12 h. Subsequently, we assayed the effects of non-cytotoxic concentrations of Pb which are detected in human blood on human lymphocytes and investigated if Pb can affect oxidative stress and cellular organelles at these concentrations. So, in concentrations which have no cytotoxic effects, Pb is shown to induce oxidative stress in addition to inflicting damage on mitochondria and lysosomes in human blood lymphocytes.

The role of heavy metals such as lead (Pb) and cadmium (Cd) in the etiology of many diseases has been proven. Also, these heavy metals can affect the normal mitochondrial function. Mitochondrial administration therapy is one of the methods used by researchers to help improve mitochondrial defects and diseases. The use of isolated mitochondria as a therapeutic approach has been investigated in in vivo and in vitro studies. Accordingly, in this study, the effects of mitochondrial administration on the improvement of toxicity caused by Pb and Cd in renal proximal tubular cells (RPTC) have been investigated. The results showed that treatment to Pb and Cd caused an increase in the level of free radicals, lipid peroxidation (LPO) content, mitochondrial and lysosomal membrane damage, and also a decrease in the reduced glutathione content in RPTC. In addition, reports have shown an increase in oxidized glutathione content and changes in energy (ATP) levels. Following, the results have shown the protective role of mitochondrial administration in improving the toxicity caused by Pb and Cd in RPTC. Furthermore, the mitochondrial internalization into RPT cells is mediated through actin‐dependent endocytosis. So, it could be suggested that the treatment of Pb‐ and Cd‐induced cytotoxicity in RPTC could be carried out through mitochondria administration. [ABSTRACT FROM AUTHOR]

Retinoblastoma (RB) is one of the most important cancers in children with a higher rate of prevalence in developing countries. Despite different approaches to the treatment of RB, it seems necessary to discover a new approach to its treatment. Today, mitochondria are recognised as an important target in the treatment of cancer. Superparamagnetic iron oxide nanoparticles (SPIONs) have been studied by researchers due to their important biological effects. In this study, the effects of SPIONs on mitochondria isolated from Y79 retinoblastoma cells were investigated. The results showed that SPIONs were able to increase the reactive oxygen species (ROS) level and subsequently damage the mitochondrial membrane and release cytochrome c a as one of the important pro-apoptotic proteins of RB mitochondria. Furthermore, the results indicated a decrease in cell viability and an increase in caspase-3 activity in Y79 retinoblastoma cells. These events can lead to the killing of cancerous mitochondria. Our results suggest that SPIONs can cause mitochondrial dysfunction and death in RB mitochondria. [ABSTRACT FROM AUTHOR]

One of the important issues in urban areas is air pollution which causes respiratory disorders. A signifi cant association between exposure to inhaled particulate matter (PM), mainly ultrafi ne particles, and increased neurological and pulmonary morbidity and mortality was observed in some research. This study aimed to demonstrate the relation between multi-wall carbon nanotubes (MWCNTs) inhalation and the carcinogenic effect of these materials in the brain and lungs. For this purpose, we investigated gene expression in rat brain and lung tissues induced by exposure to MWCNTs. Rats were exposed to MWCNTs in diameters of 10 and 100 nm (pure and impure) at a concentration of 5 mg/m3 . Exposure was done through a whole-body exposure chamber for 5 h/day, 5 days/week for 14 days. After exposure, both brain and lung tissues were isolated to evaluate certain gene expressions including Bax, Bcl2, Rac1, Tp53, Mmp12, and Arc. The results showed that exposure to impure and pure MWCNTs (10 and 100 nm) at a concentration of 5 mg/m3 causes up-regulation or down-regulation of some of these genes. The results suggest that impure and pure MWCNTs (10 and 100 nm) can increase the risk of central nervous system disorders such as Alzheimer’s disease and increase the risk of carcinogenesis in the lung tissues of rats exposed to MWCNTs (Tab. 2, Fig. 2, Ref. 64). Text in PDF www.elis.sk. [ABSTRACT FROM AUTHOR]