Corrections to: ‘‘Age distribution of cancer in mice’’Harding, Charles; Pompei, Francesco; Wilson, Richard
doi: 10.1177/0748233710386410pmid: 20947655
Abstract We found a crucial error in an earlier paper on cancer in elderly mice, Age distribution of cancer in mice: the incidence turnover at old age (Pompei et al., 2001). That paper’s principal data set, the ED01 records, was scrambled when read and analyzed with a statistical software package. Having done our best to correct the error, and having subjected the data to a more exact extension of originally published methods, we arrive at conclusions significantly different from those proposed in the original article. What appeared to be a dramatic fall off of the cancer mortality rate in mice over 2 years of age is now found to be a continuation or flattening of approximately exponential growth. This new finding is entirely at odds with the old, and does not support our later work on humans. Two of this paper’s authors, F Pompei and R Wilson, contributed to the original article. We are informing authors who have cited our paper in the past and apologize deeply for any wasted time or lost work. We should have subjected the ED01 records to more error checks. We thank Jennifer Blank for helping us discover and correct this error. The ED01 records and our earlier research are available http://physics.harvard.edu/∼wilson/cancer&chemicals/ED01.
Factors affecting exhaled carbon monoxide levels in coffeehouses in the Western Black Sea region of Turkey: Bahcebasi, Talat ;Kandis, Hayati ;Baltaci, Davut ;Kara, İsmail Hamdi
doi: 10.1177/0748233710383888pmid: 20858650
The aim of this study was to evaluate indoor air quality and factors affecting expired carbon monoxide (CO) levels in a coffeehouse environment. This cross-sectional study was conducted at 16 randomly selected coffeehouses in Duzce, Turkey, during November 2007 to March 2008. A total of 547 people, average age 46.72 ± 17.03 (19—82) years, participated. The selected coffeehouses were divided into four groups: (1) smoking, (2) nonsmoking, (3) old-style and (iv) new-style coffeehouses. Prior to entering the coffeehouse, exhaled CO levels in smokers (mean 21.17 ± 6.73 parts per million [ppm]) were significantly higher than those for nonsmokers (6.51 ± 4.56 ppm; p < 0.001). Measurements taken after 2 hours in the coffeehouse also showed significantly higher CO concentrations for smokers (22.72 ± 5.31 ppm), compared to nonsmokers (6.51 ± 4.56 ppm; p < 0.001). It was determined that CO levels inside coffee shops were above the WHO guidelines. Exhaled CO levels in nonsmokers are influenced by the ambient CO levels as a result of the use of cigarettes in coffeehouses in addition to the structure of coffeehouses.
Effects of Melissa officinalis L. on oxidative status and DNA damage in subjects exposed to long-term low-dose ionizing radiation: Zeraatpishe, Akbar ;Oryan, Shahrbano ;Bagheri, Mohammad Hadi;Pilevarian, Ali Asghar;Malekirad, Ali Akbar;Baeeri, Maryam ;Abdollahi, Mohammad
doi: 10.1177/0748233710383889pmid: 20858648
The aim of this study was to determine the capability of Melissa officinalis L. (Lemon balm) infusion on improvement of oxidative stress status in radiology staff that were exposed to persistent low-dose radiation during work. The study was a before-after clinical trial performed on 55 radiology staff. They were asked to drink Lemon balm infusion which was prepared like a tea bag twice daily (1.5 g/100 mL) for 30 days. In the plasma, lipid peroxidation, DNA damage, catalase, superoxide dismutase, myeloperoxidase, and glutathione peroxidase activity were measured before and after using Lemon balm infusion.Use of Lemon balm infusion in radiology unit workers resulted in a significant improvement in plasma levels of catalase, superoxide dismutase, and glutathione peroxidase and a marked reduction in plasma DNA damage, myeloperoxidase, and lipid peroxidation. It is concluded that infusion of Lemon balm markedly improve oxidative stress condition and DNA damage in radiology staff when used as a dietary supplement for radiation protection.
Adverse effects of exposure to low doses of chlorpyrifos in lactating rats: Mansour, Sameeh A ;Mossa, Abdel-Tawab H
doi: 10.1177/0748233710384054pmid: 20870695
This study was conducted to shed light on the effect of exposure of lactating rat to chlorpyrifos (CPF). CPF was orally administered to lactating rats at 0.01 mg kg-1 b.wt. (acceptable daily intake, ADI), 1.00 mg kg-1 b.wt. (no observed adverse effects level, NOAEL) and 1.35 mg kg-1 b.wt. (1/100 LD 50) from postnatal day 1 (PN1) until day 20 (PN20) after delivery. Results indicated decreases in body weight and increases in relative liver and kidney weights of exposed dams. Significant damage to liver was observed via increased plasma levels of aminotransferases (aspartate aminotransferase (AST) and alanine aminotransferase (ALT)) lactate dehydrogenase (LDH) and γ-glutamyle transferase (γ-GT) in a dose-dependent manner. At two high doses of CPF (1.00 and 1.35 mg kg-1 b.wt.), the lactating mothers showed significant decrease in the activity of cholinesterase (ChE). Lipid peroxidation was significantly increased, while glutathione s-transferase (GST) and superoxide dismutase (SOD) were significantly decreased compared to control. At high dose of CPF (1.35 mg kg-1 b.wt.), total protein and uric acid levels were significantly increased. CPF caused dose-related histopathological changes in liver and kidney of the CPF-treated dams.
Biomarker expression in lung of rabbit with pulmonary fibrosis induced by ammonium perchlorate: Wu, Feng-hong ;Guo, Hui-xia ;Lin, Ming-fang ;Chen, Zhi-ze ;Zhou, Xuan;Peng, Kai-liang
doi: 10.1177/0748233710386406pmid: 20937628
Ammonium perchlorate (AP), an oxidizer, has been used in solid propellants. Although AP exposure has been suspected as a risk factor for the development of pulmonary fibrosis, data are still inconclusive. To evaluate the pulmonary toxicity and the potential pulmonary fibrosis caused by occupational exposure to this compound, 25 male rabbits were randomly allocated into five groups to receive AP or bleomycin or saline by intratracheal injection. All rabbits were sacrificed and total RNA from the lungs was extracted. Expressions of types I and III collagens, transforming growth factor-β1 (TGF-β1) and tumour necrosis factor-α (TNF-α) messenger RNA (mRNA) were measured by reverse transcription-polymerase chain reaction (RT-PCR). The expressions of type I and III collagen mRNA in low, moderate and high dose AP groups were significantly higher (p < 0.01 or p < 0.05) than that in the saline group. There was also a significant increased level of TGF-β1 and TNF-α mRNA in the three AP groups compared with saline control group (p < 0.01 or p < 0.05). These results reveal that AP can increase gene expressions of types I, III collagens, TGF-β1 and TNF-α in lung of rabbits exposed to AP. The overexpression of these biomarkers were considered as effective indicator linking to the development of pulmonary fibrosis and finally demonstrated that AP has potential to induce pulmonary fibrosis.
Asthenopia (eyestrain) in working children of gem-polishing industries: Tiwari, Rajnarayan R ;Saha, Asim ;Parikh, Jagdish R
doi: 10.1177/0748233710386407pmid: 20940266
Working children of gem-polishing units are exposed to poor illumination and improper workstations. Also processes require lot of visual and mental concentration for precision. This may result in eyestrain. The study included 432 exposed and 569 comparison group subjects. Self-reported eyestrain was recorded through personal interview. Eyestrain included symptoms like itching, burning, or irritated eyes; tired or heavy eyes; difficulty seeing clearly (including blurred or double vision); and headache. The study variables included age, gender, daily working hours, and duration of exposure. The prevalence of eyestrain in child labourers was 32.2%, which was significantly more than the comparison group subjects. Also, the working children of gem-polishing units were at 1.4 times higher risk of developing eyestrain. Age 314 years and female gender were significantly associated with the eyestrain. The prevalence of eyestrain in child labourers was 32.2% and was associated with age 314 years and female gender.
Roles of reactive oxygen species and mitochondria in cadmium-induced injury of liver cells: Liu, Tao;He, Wenting;Yan, Chuan;Qi, Yongmei;Zhang, Yingmei
doi: 10.1177/0748233710386408pmid: 21148202
The roles of reactive oxygen species (ROS) and mitochondrial damage in the cadmium (Cd)-induced injury of liver cells were studied by using N-acetyl-L-cysteine (NAC) and acetyl-L-carnitine hydrochloride (ALCAR). After exposure of experimental rats to cadmium (Cd) for 16 h, mitochondrial membrane potential (MMP), ROS production, glutathione peroxidase (GSH-Px) activity, glutathione (GSH) content, malondialdehyde (MDA) content and DNA single-strand break (DNA-SSB) were analyzed. Loss of MMP, increase of ROS production, inhibition of GSH-Px activity, elevation of GSH content, rise of MDA content and DNA-SSB level suggest the participation of ROS and mitochondrion in Cd-induced injury of liver cell. NAC pretreatment attenuated oxidative stress, reversed the decline in GSH-Px activity and reduced GSH and MDA levels significantly. However, Cd-induced loss in MMP was significantly exacerbated by NAC. For another, ALCAR did not perform as well as NAC in terms of reducing ROS production, restoring GSH-Px activity and reducing GSH content. Nevertheless, it significantly improved the recovery of MMP and reduction of MDA content. In addition, conspicuous DNA damage was observed in the samples treated with NAC or ALCAR, indicating Cd could attack DNA through other pathways. These results suggest that oxidative stress or mitochondrial impairment plays a main role in different injuries respectively.
Thyroid functions in paints production workers and the mechanism of oxidative-antioxidants status: Saad-Hussein, Amal ;Hamdy, Hanaa ;Aziz, Hisham M ;Mahdy-Abdallah, Heba
doi: 10.1177/0748233710386409pmid: 20937627
Assessment of occupational exposure to paints production chemicals mainly organic solvents in production of thyroid dysfunction and the mechanism of oxidative-antioxidant imbalance. Triiodothyronine (T3), thyroxine (T4), malondialdehyde (MDA), nitric oxide (NO) and total antioxidants was measured in 36 workers and 40 controls. T3 and T4 were elevated in 18.8% and 44.4% of the workers, respectively. T3, T4, MDA and NO levels were significantly higher in workers compared to controls. Total antioxidants was significantly lower in workers than in controls. T3 and T4 were significantly correlated with duration of exposure, while, total antioxidants was inversely correlated. In workers, T3 was significantly correlated with MDA and inversely correlated with total antioxidants levels. MDA and NO were significantly higher in workers with abnormal T 4 than normal workers. Workers exposed to organic solvents proved to be at risk for hyperthyroidism. Oxidative-antioxidant imbalance was found to have a significant role in development of hyperthyroidism with increasing duration of exposure.
P53 and Bcl2 apoptosis proteins in meso-2,3-dimercaptosuccinic acid treated lead-intoxicated rabbits: Tousson, Ehab ;Rafat, Bassem M ;Hessien, Mohamed ;Barbary, Ahmed A El;Sami, Ahmed
doi: 10.1177/0748233710386411pmid: 21112928
Lead (Pb) toxicity is one of the commonest environmental problems in our life; it causes many reversible and irreversible changes in our tissues. This study was carried out to investigate the effect of meso-2,3-dimercaptosuccinic acid (DMSA) on treatment of oxidative stress caused by lead poisoning in rabbits. Lead acetate (Pb(Ac)2) was orally administrated to rabbits for 21 days and then treated by DMSA for another 21 days. The effect of this treatment was investigated by measuring 2 of the apoptosis proteins p53 and Bcl2. Also, the auto-oxidation rate and their histopathological changes in brain, bone and liver were investigated. Hemoglobin auto-oxidation rate is measured as well as histopathological study of liver. Our data indicate that exposure to rabbits to Pb(Ac)2 caused a significant increase of apoptosis protein p53 and decrease in the antiapoptotic BCl2 proteins.