Oxidative stress and its correlation with nuclear factor-κB and transforming growth factor-β1 in liver injury induced by different doses of X-rays in mice / 环境与职业医学

Background Radiation-induced liver damage is a major complication for primary liver cancer and other upper abdominal tumors during radiation therapy. The early biological effects of radiation-induced liver damage at different doses of radiation and its mechanisms of action have not yet been elucidated. Objective To establish X-ray-induced radioactive mouse liver damage model and explore the level of oxidative stress and its correlation with nuclear factor-κB (NF-κB) and transforming growth factor-β1 (TGF-β1). Methods A total of 24 male C57BL/6J mice aged 6 weeks were randomly divided into 4 groups (control, 0.8 Gy, 1.6 Gy, and 4 Gy), with 6 mice in each group. X-rays irradiated the whole body of mice singly in each dose group. At 24 h after radiation, histopathological changes in mouse liver were evaluated; peripheral blood cell count, serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels, as well as liver tissue superoxide dismutase (SOD) activity, malondialdehyde (MDA) level, reduced glutathione (GSH) level, and 8-hydroxy-2′-deoxyguanosine (8-OHdG) level were measured; real-time fluorescence quantitative PCR was used to detect liver tissue NF-κB p65 and TGF-β1 mRNA expression levels; the correlations of oxidative stress indicators with NF-κB p65 and TGF-β1 mRNA expression levels were analyzed by Pearson correlation. Results Compared with the control group, at 24 h after different doses of X-ray radiation, early injury-related histopathological changes were observed in liver, and the serum levels of AST and ALT were significantly increased in the 4 Gy group (P<0.05); the numbers of peripheral blood leukocytes and lymphocytes were decreased in the radiation exposure groups (P<0.05), showing a decreasing trend with increasing radiation doses; the levels of liver oxidative stress indicators (MDA, SOD, and GSH) in exposed mice were significantly increased (P<0.05), showing an increasing trend with increasing radiation doses. The liver 8-OHdG were significantly increased in the 1.6 Gy and 4 Gy groups compared with the control and the 0.8 Gy groups, respectively (P<0.05). The NF-κB p65 and TGF-β1 mRNA expression levels in the liver of mice were significantly increased in the 1.6 Gy and 4 Gy groups compared with the control group (P<0.05). The TGF-β1 mRNA expression level also exhibited an increasing trend with increasing radiation doses. The results of correlation analysis showed that the levels of MDA, SOD, GSH, and 8-OHdG in liver tissues were significantly and positively correlated with the expression levels of NF-κB p65 and TGF-β1 mRNA (P<0.05). Conclusion X-rays of various doses can affect the degree of liver injury, peripheral blood cell count, serum levels of AST and ALT, and liver oxidative stress levels in mice. The level of oxidative stress induced by X-ray is positively correlated with NF-κB and TGF-β1 in liver tissues, and it may participate in the process of radiation-induced liver injury.

Induction of Endoplasmic Reticulum Stress by Cadmium and Its Regulation on Nrf2 Signaling Pathway in Kidneys of Rats / 生物医学与环境科学（英文）

OBJECTIVE@#This study was conducted to investigate the regulation of endoplasmic reticulum stress on Nrf2 signaling pathway in the kidneys of rats.@*METHODS@#Rats were divided into twelve groups of six animals each. Some groups were pre-administered with bacitracin or tauroursodeoxycholic acid (TUDCA), and all of them were treated with 5-20 μmol/kg cadmium (Cd) for 48 h. The oxidative stress levels were analyzed using kits. The mRNA and protein expression levels of endoplasmic reticulum stress-related factors and Nrf2 signaling pathway-related factors were determined using RT-PCR and western blot.@*RESULTS@#Cd exposure resulted in oxidative stress in the kidneys of rats and upregulated the expression of endoplasmic reticulum stress (ERS)-related factors and Nrf2 signaling pathway-related factors, especially at doses of 10 and 20 μmol/kg Cd, and the expression changes were particularly obvious. Moreover, after pretreatment with bacitracin, Cd upregulated the expression of ERS-related factors to a certain extent and, at higher doses, increased the mRNA expression of Nrf2. After pretreatment with TUDCA, Cd reduced the level of ERS to a certain extent; however, at these doses, there were no significant changes in the expression of Nrf2.@*CONCLUSION@#Cadmium can result in ERS and oxidative stress in the kidneys of rats, activate Nrf2, and upregulate the transcriptional expression of phase II detoxification enzymes under these experimental conditions. ERS has a positive regulation effect on Nrf2 signaling pathway but has little effect on the negative regulation of Nrf2 signaling pathway in cadmium toxicity.

Effect of DNA single strand breaks and 8-OHd G production on cadmium-induced toxicity on human embryonic kidney epithelial cells / 中国职业医学

OBJECTIVE: To explore the effects of cadmium chloride( CdCl_2) on DNA single strand breaks and the production of 8-hydroxy-2'-deoxyguanosine( 8-OHdG) in human embryonic kidney epithelial cells( HEK cells). METHODS: HEK cells in logarithm growth phase were divided into 5 groups and incubated with the different concentrations of CdCl_2( 0. 0,2. 5,5. 0,10. 0 and 20. 0 μmol/L) for 24,48 and 72 hours in vitro. After harvesting the cells,DNA single strand breaks was tested by single cell gel electrophoresis,and the level of 8-OHdG was measured using the enzyme linked immunosorbent assay. RESULTS: The Olive tail moment was statistically significant in the main effect of CdCl_2 exposed HEK cells( P < 0. 01). Among them,when HEK cells were exposed to 5. 0 μmol / L of CdCl_2,the Olive tail moment began to have a statistical significant increasing trend compared with the 0. 0 μmol / L group( P < 0. 05); when CdCl_2 concentration was 2. 5-10. 0 μmol / L,the Olive tail moment lengthened with the increasing dose of cadmium exposure,showing a doseeffect relationship( P < 0. 05). The tail DNA% was statistically significant in the interaction between exposure treatment and exposure time in HEK cells( P < 0. 01). Among them,when CdCl_2 concentration was at 2. 5-10. 0 μmol / L at 24 hours time point and 5. 0-20. 0 μmol / L at 48 hours time point,the tail DNA% raised with the increasing dose of cadmium exposure,showing a dose-effect relationship( P < 0. 05). The tail DNA% at 3 time points of 24,48 and 72 hours after exposure to 20. 0 μmol / L of CdCl_2 in HEK cells increased with the increasing time of cadmium exposure,showing a timeeffect relationship( P < 0. 05). The level of 8-OHdG had statistical significance in the main effect of CdCl_2 exposure treatment in HEK cells( P < 0. 05). Among them,the level of 8-OHdG was first significantly increased only after exposure to 10. 0 μmol / L CdCl_2 compared with the 0. 0 μmol / L group( P < 0. 05). After treatment with Ca Cl2,there was no doseeffect relationship and time-effect relationship found between the cadmium chloride exposure and tail length as well as the tail / head length ratio and 8-OHdG level. CONCLUSION: To a certain extent,CdCl_2 exposure may cause both DNA single strand breaks and 8-OHdG production in HEK cells. Compared with 8-OHdG,the DNA single strand breaks show more significant change with a lower dose of cadmium treatment,which may be related to its higher sensitivity to cadmium toxicity than 8-OHdG.

Effects of fluoride on Fas signal pathway in rat incisor cells / 中华口腔医学杂志

<p><b>OBJECTIVE</b>To investigate the effects of fluoride on Fas expression, caspase-3 and caspase-8 activity and apoptosis in rat incisor cells.</p><p><b>METHODS</b>Forty male SD rats were divided into 4 groups randomly and provided with distilled water containing NaF at the doses of 0, 10, 50 and 100 mg/L respectively. Each group had 10 animals. Five animals were sacrificed at 60 and 90 days respectively. Fas expression was measured with immunohistochemistry, and colorimetric assay was used to examine caspase-3 and caspase-8 activity with enzyme-labelled meter. The apoptosis was detected by flow cytometry in mandibular incisor cells.</p><p><b>RESULTS</b>NaF at the doses of 10, 50 and 100 mg/L for 60 d and 90 d caused Fas overexpression, promoted activity of caspase-3 and caspase-8, increased apoptosis rate in mandibular incisor cells. At 60 days, the value of Fas expression was 0.1819 ± 0.0025 for control, 0.2120 ± 0.0084 for 10 mg/L NaF group, 0.2283 ± 0.0183 for 50 mg/L NaF group, 0.2818 ± 0.0233 for 100 mg/L NaF group. At 90 days, the value of Fas expression was 0.2077 ± 0.0289 for control, 0.2216 ± 0.0105 for 10 mg/L NaF group, 0.2377 ± 0.0059 for 50 mg/L NaF group, 0.2775 ± 0.0088 for 100 mg/L NaF group. Statistics analysis yielded close relationship between the dose of NaF in water and the Fas expression, and also between the dose of NaF in water and caspase-3 activities, and the relative coefficient was 0.9728 (60 d, P < 0.01) and 0.9889 (90 d, P < 0.01) for Fas expression, 0.9533 (60 d, P < 0.01) and 0.9849 (90 d, P < 0.01) for caspase-3 activity respectively. Apoptosis rate and caspase-8 activity also had close relationship with the NaF doses, and the relative coefficient was 0.9733 (90 d, P < 0.01) for apoptosis, 0.9928 (90 d, P < 0.01) for caspase-8. At the doses of 10, 50 and 100 mg/L NaF for 60 d and 90 d, obvious relationship was found between Fas expression and caspase-3 activity, and the relative coefficient was 0.9619 (60 d, P < 0.01) and 0.9912 (90 d, P < 0.01). Obvious relationship between Fas expression and apoptosis, between Fas expression and caspase-8 activity was found in groups for 90 d, and the relative coefficient was 0.9841 (P < 0.01) for apoptosis, 0.9767 (P < 0.01) for caspase-8.</p><p><b>CONCLUSIONS</b>Fluoride could induce Fas overexpression and mediate caspase activation and apoptosis at the doses of 10, 50 and 100 mg/L for 60 d and 90 d in rat mandibular incisor cells.</p>

Telomerase activity and telomerase reverse transcriptase expression induced by selenium in rat hepatocytes / 生物医学与环境科学（英文）

<p><b>OBJECTIVE</b>To investigate the effects of sodium selenite on telomerase activity, apoptosis and expression of TERT, c-myc and p53 in rat hepatocytes.</p><p><b>METHODS</b>Selenium at doses of 2.5, 5.0, and 10 micromol/kg was given to SD rats by gavage. In rat hepatocytes, telomerase activity was measured by the telomeric repeat amplification protocol (TRAP), apoptosis was detected by flow cytometry, and expressions of telomerase reverse transcriptase (TERT), c-myc and p53 were analyzed by reverse transcription-polymerase chain reaction (RT-PCR). c-Myc and P53 proteins were detected by immunochemistry.</p><p><b>RESULTS</b>Selenium at doses of 2.5, 5.0, and 10 micromol/kg significantly increased hepatocellular telomerase activity and induced apoptosis in a dose-dependent manner. Although selenium at doses of 2.5, 5.0, and 10 micromol/kg displayed no obvious enhancing effect on the TERT mRNA expression in rat hepatocytes (P > 0.05), it significantly increased the c-myc mRNA and p53 mRNA expression at the dose of 10 micromol/kg (P < 0.05). Selenium at doses of 5.0 and 10 micromol/kg obviously increased the content of P53 protein in rat hepatocytes, but only at the dose of 10 micromol/kg, it significantly promoted the value of c-Myc protein in them.</p><p><b>CONCLUSION</b>Selenium can slightly increase telomerase activity and TERT expression, and significantly induce apoptosis and over-expression of c-myc and p53 at relatively high doses. The beneficial effects of selenium on senescence and aging may be mediated by telomerase activation and expression of TERT, c-myc, and p53 in rat hepatocytes.</p>

Inhibitory effects of selenium on telomerase activity and hTERT expression in cadmium-transformed 16HBE cells / 生物医学与环境科学（英文）

<p><b>OBJECTIVE</b>To investigate the effects of sodium selenite on telomerase activity and expression of hTERT mRNA in cadmium-transformed 16HBE cells.</p><p><b>METHODS</b>Telomerase activity and expression of genes were measured after cultured cadmium-transformed 16HBE cells were exposed to sodium selenite at different doses (0.625, 1.25, 2.50, 5.00 micromol/L) for 24 hours.</p><p><b>RESULTS</b>Selenium decreased telomerase activity in cadmium-transformed 16HBE cells. There existed an obvious dose-effect relationship between the selenium concentration and these changes. The expression of hTERT and c-myc mRNA also decreased but the expression of mad1 mRNA increased after exposure to selenium for 24 hours. No difference was found in expression of hTRF1 and hTRF2 mRNA after incubated with sodium selenite for 24 hours, compared with control group.</p><p><b>CONCLUSION</b>Selenium inhibits telomerase activity by decreasing hTERT and c-myc mRNA expression and increasing mad1 mRNA expression in cadmium-transformed 16HBE cells and selenium concentration is significantly correlated with these changes.</p>

Effects of cadmium on hepatocellular DNA damage, proto-oncogene expression and apoptosis in rats / 生物医学与环境科学（英文）

<p><b>OBJECTIVE</b>To study the effects of cadmium on hepatocellular DNA damage, expression of proto-oncogenes c-myc, c-fos, and c-jun as well as apoptosis in rats.</p><p><b>METHODS</b>Cadmium chloride at the doses of 5, 10, and 20 micromol/kg was given to rats by i.p. and there were 5 male SD rats in each group. Hepatocellular DNA damage was measured by single cell gel electrophoresis (or comet assay), while expression of proto-oncogenes c-myc, c-fos, and c-jun in rat hepatocytes were measured by Northern dot hybridization. C-Myc, c-Fos, and c-Jun were detected with immuno-histochemical method. Hepatocellular apoptosis was determined by TUNEL (TdT-mediated dUTP Nick End Labelling) and flow cytometry.</p><p><b>RESULTS</b>At the doses of 5, 10, and 20 micromol/kg, cadmium chloride induced DNA damage in rat hepatocytes and the rates of comet cells were 50.20%, 88.40%, and 93.80%, respectively. Results also showed an obvious dose-response relationship between the rates of comet cells and the dose of cadmium chloride (r = 0.9172, P < 0.01). Cadmium chloride at the doses of 5, 10, and 20 micromol/kg induced expression of proto-oncogenes c-myc, c-fos, and c-jun. The positive brown-yellow signal for c-myc, c-fos, and c-jun was mainly located in the cytoplasm of hepatocytes with immunohistochemical method. TUNEL-positive cells were detected in cadmium-treated rat livers. Apoptotic rates (%) of cadmium-treated liver cells at the doses of 5, 10, and 20 micromol/kg were (17.24 +/- 2.98), (20.58 +/- 1.35), and (24.06 +/- 1.77) respectively, being significantly higher than those in the control. The results also displayed an obvious dose-response relationship between apoptotic rates and the dose of cadmium chloride (r = 0.8619, P < 0.05).</p><p><b>CONCLUSION</b>Cadmium at 5-20 micromol/kg can induce hepatocellular DNA damage, expression of proto-oncogenes c-myc, c-fos, and c-jun as well as apoptosis in rats.</p>

Effects of selenium and zinc on renal oxidative stress and apoptosis induced by fluoride in rats / 生物医学与环境科学（英文）

<p><b>OBJECTIVE</b>To study the effects of selenium and zinc on oxidative stress, apoptosis, and cell cycle changes in rat renal cells induced by fluoride.</p><p><b>METHODS</b>Wistar rats were given distilled water containing sodium fluoride (50 mg/L NaF) and were gavaged with different doses of selenium-zinc preparation for six months. Four groups were used and each group had eight animals (four males and four females). Group one, sham-handled control; group two, 50 mg/L NaF; group three, 50 mg/L NaF with a low dose of selenium-zinc preparation (0.1 mg/kg Na2 SeO3 and 14.8 mg/kg ZnSO4 x 7H2O); and group four, 50 mg/L NaF with a high dose of selenium-zinc preparation (0.2 mg/kg Na2 SeO3 and 29.6 mg/kg ZnSO4 x 7H2O). The activities of serum glutathione peroxidase (GSH-Px), kidney superoxide dismutase (SOD), and the levels of malondialdehyde (MDA) and glutathione (GSH) in the kidney were measured to assess the oxidative stress. Kidney cell apoptosis and cell cycle were detected by flow cytometry.</p><p><b>RESULTS</b>NaF at the dose of 50 mg/L increased excretion of fluoride in urine, promoted activity of urine gamma-glutamyl transpeptidase (gamma-GT), inhibited activity of serum GSH-PX and kidney SOD, reduce kidney GSH content, and increased kidney MDA. NaF at the dose of 50 mg/L also induced rat renal apoptosis, reduced the cell number of G2/M phase in cell cycle, and decreased DNA relative content significantly. Selenium and zinc inhibited effects of NaF on oxidative stress and apoptosis, promoted the cell number of G2/M phase in cell cycle, but failed to increase relative DNA content significantly.</p><p><b>CONCLUSION</b>Sodium fluoride administered at the dose of 50 mg/L for six months induced oxidative stress and apoptosis, and changes the cell cycle in rat renal cells. Selenium and zinc antagonize oxidative stress, apoptosis, and cell cycle changes induced by excess fluoride.</p>

DNA damage, apoptosis and C-myc, C-fos, and C-jun overexpression induced by selenium in rat hepatocytes / 生物医学与环境科学（英文）

<p><b>OBJECTIVE</b>To study the effects of selenium on DNA damage, apoptosis and c-myc, c-fos, and c-jun expression in rat hepatocytes.</p><p><b>METHODS</b>Sodium selenite at the doses of 5, 10, and 20 micromol/kg was given to rats by i.p. and there were 5 male SD rats in each group. Hepatocellular DNA damage was detected by single cell gel electrophoresis (or comet assay). Hepatocellular apoptosis was determined by TUNEL (TdT-mediated dUTP nick end labelling) and flow cytometry. C-myc, c-fos, and c-jun expression in rat hepatocytes were assayed by Northern dot hybridization. C-myc, c-fos, and c-jun protein were detected by immunohistochemical method.</p><p><b>RESULTS</b>At the doses of 5, 10, and 20 micromol/kg, DNA damage was induced by sodium selenite in rat hepatocytes and the rates of comet cells were 34.40%, 74.80%, and 91.40% respectively. Results also showed an obvious dose-response relationship between the rates of comet cells and the doses of sodium selenite (r=0.9501, P<0.01). Sodium selenite at the doses of 5, 10, and 20 micromol/kg caused c-myc, c-fos, and c-jun overexpression obviously. The positive brown-yellow signal for proteins of c-myc, c-fos, and c-jun was mainly located in the cytoplasm of hepatocytes with immunohistochemical method. TUNEL-positive cells were detected in selenium-treated rat livers. Apoptotic rates (%) of selenium-treated liver cells at the doses of 5, 10, and 20 micromol/kg were (3.72 +/- 1.76), (5.82 +/- 1.42), and (11.76 +/- 1.87) respectively, being much higher than those in the control. Besides an obvious dose-response relationship between apoptotic rates and the doses of sodium selenite (r=0.9897, P<0.01), these results displayed a close relationship between DNA damage rates and apoptotic rates, and the relative coefficient was 0.9021, P<0.01.</p><p><b>CONCLUSION</b>Selenium at 5-20 micromol/kg can induce DNA damage, apoptosis, and overexpression of c-myc, c-fos, and c-jun in rat hepatocytes.</p>

Effects of selenium on expression of TERT, c-Myc and p53 induced by cadmium in rat liver / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To study the effects of sodium selenite on expression of telomerase reverse transcriptase mRNA, c-Myc and p53 induced by cadmium chloride in rat liver.</p><p><b>METHODS</b>Male SD rats were divided randomly into 6 groups, each group had 5 animals. The groups comprised the control group, Se group (5 micromol/kg sodium selenite), 5 micromol/kg cadmium chloride group, 10 micromol/kg cadmium chloride group, Se (5 micromol/kg sodium selenite) + 5 micromol/kg cadmium chloride group, Se (5 micromol/kg sodium selenite) + 10 micromol/kg cadmium chloride group. After 48 hours of the first injection, the expression of TERT mRNA was measured with RT-PCR and c-Myc, and p53 proteins were measured by immunohistochemistry method.</p><p><b>RESULTS</b>Compared with control group, the expression of TERT was increased in 5 micromol/kg Cd group and 10 micromol/kg Cd group, c-Myc protein was increased in 10 micromol/kg Cd group, and the expression of p53 protein was increased in 5 micromol/kg group and 10 micromol/kg Cd group. TERT expression in Se + 10 micromol/kg Cd group was lower than that of 10 micromol/kg Cd group significantly. c-Myc protein was decreased in Se + 10 micromol/kg Cd group compared with 10 micromol/kg Cd group. p53 protein of Se + 5 micromol/kg Cd group and Se + 10 micromol/kg Cd group were decreased significantly compared with 5 micromol/kg Cd group and 10 micromol/kg Cd group respectively.</p><p><b>CONCLUSION</b>The cadmium at the doses of between 5 and 10 micromol/kg can activate TERT and up-regulate c-Myc and p53 proteins. The selenium at the dose of 5 micromol/kg has the antagonistic effect on expression of TERT, c-Myc and p53 induced by cadmium in rat liver.</p>

Effects of selenium on rat hepatocellular DNA damage, apoptosis and changes of cell cycle induced by cadmium in vivo / 中华预防医学杂志

<p><b>OBJECTIVE</b>This study was conducted to study the effects of sodium selenite on rat hepatocellular DNA damage, apoptosis, changes of cell cycle and DNA relative content induced by cadmium chloride in vivo.</p><p><b>METHODS</b>Both sodium selenite at the dose of 5 micromol/kg and cadmium chloride at the dose of 5 micromol/kg, 10 micromol/kg and 20 micromol/kg were given to rats by i.p. and there were 5 male SD rats in each group. Hepatocellular DNA damage was measured by the single cell gel electrophoresis (or comet assay), hepatocellular apoptosis was measured with TUNEL (TdT-mediated dUTP Nick End Labelling) and flow cytometry, DNA relative content (DNA(RC)) and cell cycle were detected with flow cytometry.</p><p><b>RESULTS</b>When sodium selenite at the dose of 5 micromol/kg acted jointly with cadmium chloride at the dose of 5 micromol/kg, 10 micromol/kg and 20 micromol/kg respectively, the results showed that selenium reduced the effect of cadmium on DNA damage and apoptosis and decreased the rates of DNA damage and the rates of apoptosis significantly. Sodium selenite at the dose of 5 micromol/kg increased cell number of G(0)/G(1) period decreased by cadmium chloride at the dose of 5 micromol/kg and increased cell number of G(2)/M period decreased by cadmium chloride at the dose of 10 micromol/kg and 20 micromol/kg. Sodium selenite at the dose of 5 micromol/kg increased DNA relative content reduced by cadmium chloride at the dose of 10 micromol/kg and 20 micromol/kg.</p><p><b>CONCLUSIONS</b>It was suggested that selenium at certain doses could antagonize DNA damage, apoptosis, changes of cell cycle and DNA relative content induced by cadmium in rat hepatocytes in vivo.</p>

Effects of selenium on rat hepatocellular DNA damage induced by cadmium in vitro / 中华预防医学杂志

<p><b>OBJECTIVES</b>This study was conducted to explore effects of selenium on rat hepatocellular DNA damage induced by cadmium in vitro.</p><p><b>METHOD</b>Sodium selenite was added at concentrations of 8.75, 17.50 and 35.00 micromol/L respectively with cadmium chloride at the concentrations of 8.75, 17.50 and 35.00 micromol/L respectively and rat hepatocellular DNA damage was measured with single cell gel electrophoresis (comet assay).</p><p><b>RESULTS</b>Sodium selenite at the concentration of 8.75 micromol/L inhibited DNA damage caused by cadmium chloride at the concentration of 8.75, 17.50 and 35.00 micromol/L in rat liver cells (P < 0.05). Although sodium selenite at 17.50 micromol/L inhibited DNA damage induced by cadmium chloride at 17.50 and 35.00 micromol/L, it did not inhibit DNA damage induced by cadmium chloride at 8.75 micromol/L. Sodium selenite at 35.00 micromol/L did not have antagonistic effects on DNA damage induced by cadmium chloride at 8.75, 17.50 and 35.00 micromol/L. In addition, sodium selenite at 8.75 micromol/L had the best antagonistic effect while cadmium chloride at 8.75 micromol/L, but the antagonistic effect of sodium selenite at 17.50 micromol/L was better than 8.75 micromol/L while cadmium chloride at 17.50 and 35.00 micromol/L.</p><p><b>CONCLUSION</b>The antagonistic effect of selenium on rat hepatocellular DNA damage induced by cadmium related to the concentrations of selenium and also to the concentration ratio between selenium and cadmium.</p>

Effects of selenium on benzoa pyrene-induce DNA damage in mouse lung cells / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To explore the effects of selenium on DNA damage induced by benzo[a] pyrene (BaP) in mouse lung cells.</p><p><b>METHODS</b>Sodium selenite was given to Kunming male mice by i.p. and BaP was given by oral gavage. The control group was given solvent only with the same method. DNA damage was detected by single cell gel electrophoresis (or comet assay).</p><p><b>RESULTS</b>The damage degrees in mice treated with 125, 250 and 500 mg/kg of BaP were more severe than that of control (P < 0.01). The rates of comet cells in the BaP-treated groups (43.50%, 84.00%, 95.63%) were significantly higher than that of control (9.75%, P < 0.01), and there was obvious dose-response relationship. 0.75, 1.50 and 3.00 mg/kg of sodium selenite presented antagonistic effects against DNA damage induced by 250 mg/kg of BaP in mouse's lung cells. The antagonistic effect of sodium selenite at the dose of 1.50 mg/kg was better than those of sodium selenite at the doses of 0.75, 3.00 mg/kg.</p><p><b>CONCLUSION</b>BaP at the doses of 125 approximately 500 mg/kg could significantly induce DNA damage of lung cells in mice. 0.75 approximately 3.00 mg/kg of sodium selenite could inhibit DNA damage of lung cells in mice induced by 250 mg/kg of BaP.</p>