Toxicology and Industrial Health

Arif, Mohammad; Islam, MM Towhidul; Shekhar, Hossain Uddin

doi: 10.1177/0748233717754163pmid: 29519200

Lead exposure can damage cells directly by effecting DNA or indirectly by modifying proteins and enzymes. In Bangladesh, many working children are exposed to a very high level of lead during their early life due to their involvement with lead-oriented professions. This imposes a severe threat to the growth and development of the children. Therefore to study the effect of lead, we enrolled 60 age-matched male children, from an area of old Dhaka city, where battery-recycling shops are located, depending on their blood lead concentration. If the children had a plasma lead concentration above the WHO recommended threshold level of 10 µg/dl, we grouped them as test subjects and others as control subjects to determine the effect of lead on different biochemical parameters of the body. Compared to the controls, acculumlation of the lipid peroxidation product, malondialdehyde, increased significantly in test subjects (p < 0.01). Lead exposure also increased the protein carbonyl content (p < 0.05) and significantly decreased the plasma glutathione levels of test subjects compared to the controls (p < 0.05). While comparing the lead-exposed group against controls, it was found that the percentage of damaged DNA, as measured using the Comet assay, significantly increased in tail (p < 0.01) and decreased in head regions. All of these results suggest that high-plasma lead content may induce an oxidative stress to the study population, which may lead to DNA damage.

Wang, Chong; Chen, Yan; Manthari, Ram Kumar; Wang, Jundong

doi: 10.1177/0748233718754471pmid: 29529942

cAMP response element modulator (CREM) is involved in regulating gene expression in normal spermatogenesis. The transcriptional activity of CREM is partly regulated by activator of CREM in the testis (ACT). To investigate the effects of different concentrations of sodium fluoride (NaF) on the gene and protein expression of CREM and ACT in the mouse testis, sexually mature male Kunming mice were exposed to 50, 100, or 150 mg/L NaF in their drinking water for 90 days. NaF reduced the sperm count and viability and increased the percentage of malformed sperm in a dose-dependent manner. The mRNA expression of CREM and ACT was markedly downregulated in the NaF-treated groups. Furthermore, immunohistochemistry revealed that CREM and ACT proteins were decreased significantly in the 50, 100, and 150 mg/L NaF-treated groups compared to the control group. These findings indicate that the decreased gene and protein expression of CREM and ACT in the testis is associated with an impairment of reproductive functions by NaF.

Gül, Semir; Gül, Mehmet; Yigitcan, Birgül

doi: 10.1177/0748233717754174pmid: 29529941

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is a toxic agent and has disruptive effects on reproductive tissues in females. TCDD disrupts the hormonal regulation of the body and decreases the production of melatonin. In this study, we investigated the protective effects of melatonin supplements against the toxic effects of TCDD on ovaries of female rats. TCDD caused a significant decrease in the average number of corpora lutea and follicles per tissue section (2.1 ± 0.7; 2.3 ± 0.8, respectively), whereas these numbers were maintained in the melatonin supplemented group (5.0 ± 0.8; 5.1 ± 0.8, respectively) and were similar to the control group (5.3 ± 1.0; 5.9 ± 0.9, respectively). Electron microscopic analysis showed that the disruption of ultrastructure components such as cell membrane and organelles due to TCDD exposure was inhibited by melatonin supplements. This study suggested that melatonin has a protective and a possible ameliorative effect over histopathological damage of rat ovaries exposed to TCDD.

Miranowicz-Dzierżawska, Katarzyna

doi: 10.1177/0748233717752090pmid: 29519201

The aim of this study was to assess whether there are differences between the results of determining oxidative stress markers obtained from different origin cell lines after exposure to chemicals generating free radicals. The studies considered two markers of oxidative stress: the level of thiobarbituric acid reactive substances (TBARS) and superoxide dismutase activity. The evaluation was performed in five cell lines: Chinese hamster ovary (CHO-9) cells, lung adenocarcinoma A549, macrophages RAW264.7, skin carcinoma cells A431, and keratinocytes HaCaT. Three compounds generating free radicals were used as a source of reactive oxygen/nitrogen: 2,2′-azobis-2-methyl-propanimidamide dihydrochloride (AAPH), sodium persulfate (SP), and 3-morpholinosydnonimine hydrochloride (SIN-1). The most appropriate cell line to assess the level of TBARS proved to be the murine macrophage cell line RAW 264.7. Equally, good performance was observed in the lung cancer cell line A549, but only when tested with AAPH and SP. In the case of measuring superoxide dismutase activity, it appeared that the most suitable cell line was also the RAW 264.7 line, although dispersion increased significantly at the highest concentrations of AAPH and SP measurements. When choosing a cell line to determine oxidative stress, the specificity of the stress-inducing compound and the parameter determined should be taken into consideration.

Huang, Bing-Fang; Chang, Ya-Chi; Han, Ai-Ling; Hsu, Hui-Tsung

doi: 10.1177/0748233717754173pmid: 29514563

The present study combined air sampling with pulmonary function tests (PFTs) to determine both the extent of air pollution proximal to an electric arc furnace (EAF) and its impact on human health. The mass concentrations of particulate matter with aerodynamic diameters less than 2.5 µm (PM2.5) in exposure areas were not significantly higher than the samples taken at a control area. However, the concentrations of five metal elements, Cd, Cr, Cu, Ni, and Zn in PM2.5 were significantly higher in the exposure area than that of the control area. PFTs showed that the average forced vital capacity (FVC) of boys was decreased with decreasing distance from the EAF factory. With normalization of pulmonary function by age, height, and weight, we found that the FVC became more negative with a decrease in distance from the EAF. Lastly, regression analysis was performed to analyze the impact of the concentrations of the five metals in PM2.5 on the performance of pulmonary function. The results showed that the metals can be ranked from the highest to the lowest in terms of impact on the FVC of boys as follows: Cr, Cd, Ni, Cu, and Zn. This finding is consistent with the ranking of metal toxicity reported in the literature for a rat lung epithelial cell line. The results of this study showed that only measuring PM2.5 mass concentrations may not provide a full explanation of its toxicity and health effects. The chemical composition of the PM2.5 can be an important factor that determined the health impact of PM2.5.

Dahlgren, James G; Talbott, Patrick J

doi: 10.1177/0748233717750982pmid: 29554820

We report two cases of formaldehyde-containing hair straighteners causing new onset asthma. Formaldehyde has been reported to cause asthma in other settings. The purpose of this article is to examine two cases of asthma in hairdressers exposed to hair smoothing products and to review the relevant literature on formaldehyde exposure and asthma. The results indicated that both subjects developed asthma from repeated occupational exposure to formaldehyde during hair treatments. Both subjects became unable to tolerate hair straightening activity in their vicinity. Formaldehyde-containing hair smoothing products are sources of exposure, and the risk of developing asthma is high in salon settings where hair straightening is performed using formaldehyde.

Sun, Shuqiang; Zhang, Chunxiao; Gao, Jiahao; Qin, Qiongyu; Zhang, Yaya; Zhu, Hua; Yang, Xinjun; Yang, Dongren; Yan, Hongtao

doi: 10.1177/0748233717750983pmid: 29506454

Benzene exposure affects the hematopoietic system and leads to the occurrence of various types of leukemia and hematotoxicity. It has been confirmed that active metabolites of benzene, including 1,4-benzoquinone (1,4-BQ), can induce reactive oxygen species (ROS) and apoptosis in the bone marrow, and recent studies have also suggested that benzene exposure can affect mitochondrial function in both experimental animals and cell lines. However, the potential relationship among ROS production, mitochondrial damages, and subsequent apoptosis following benzene exposure has not been well studied in detail. In the present study, we utilized HL-60 cells, a well-characterized human myeloid cell line, as an in vitro model and examined the effects of 1,4-BQ on intracellular ROS formation, mitochondria damage, and the occurrence of apoptotic events with or without using the ROS scavenger N-acetyl-l-cysteine (NAC). The results demonstrated that 1,4-BQ could dose-dependently induce production of ROS and mitochondrial damage as characterized by mitochondrial membrane potential disruption, mitochondrial ultrastructure alteration, and induced apoptosis and activated caspase-3 and caspase-9. Preincubation of HL-60 cells with NAC prior to 1,4-BQ treatment could block 1,4-BQ-induced production of ROS and the occurrence of apoptosis. These results demonstrated that 1,4-BQ induced apoptosis in HL-60 cells through a ROS-dependent mitochondrial-mediated pathway.