Evaluation of DNA damage in construction-site workers occupationally exposed to welding fumes and solvent-based paints in Turkey.

In this study, the comet assay was used to evaluate whether welding fume and solvent base paint exposure led to DNA damage in construction-site workers in Turkey. The workers (n = 52) were selected according to their exposure in the construction site and controls (n = 26) from the general population, with no history of occupational exposure. The alkaline comet assay, a standard method for assessing genotoxicity, has been applied in peripheral lymphocytes of all subjects. The mean percentages of DNA in tail (%DNA(T)) of each group were evaluated, including the comparisons between smokers in each different group and the duration of exposure. Significant increase in the mean %DNA(T) (p < 0.01) was observed in all exposed subjects (12.34 ± 2.05) when compared with controls (6.64 ± 1.43). Also %DNA(T) was significantly high (p < 0.01) in welders (13.59 ± 1.89) compared with painters (11.10 ± 1.35). There was a statistical meaningful difference in % DNA(T) between control and exposed smokers. Our findings indicate that exposure to welding fumes and paints induce genotoxic effect in peripheral lymphocytes, indicating a potential health risk for workers. Therefore, to ensure maximum occupational safety, biomonitoring is of great value for assessing the risk for construction workers.

Comparision of biocompatibility and cytotoxicity of two new root canal sealers.

The aim of this study was to investigate the remote organ toxicity and connective tissue reaction of two new root canal sealers ("GuttaFlow(®)" and "EndoREZ(®)") and to compare them with zinc oxide eugenol sealer using biochemical and histopathological parameters. A total of 60 white albino Wistar rats were used in the study. 0.1ml of GuttaFlow(®), EndoREZ(®) or Kerr Pulp Canal Sealer(®) were administered subcutaneously into the mid-dorsal thoracic region of rats (15 in each group). Control rats were given saline only. Rats were decapitated after 24h, on day 7 and on day 30 of the experiment and tissue samples from lung, liver, kidney and skin were removed for the determination of malondialdehyde (MDA) and glutathione (GSH) levels. In parallel, tissues were also examined histologically. Serum aspartate aminotransferase (AST), alanine aminotransferase (ALT) levels, and creatinine and blood urea nitrogen (BUN), concentrations (BUN) were measured to assess liver and kidney functions, respectively. Tumor necrosis factor (TNF) and lactate dehydrogenase (LDH) were also assayed in serum samples. No statistical differences were found among the control and EndoREZ(®), GuttaFlow(®) and Kerr Pulp Canal sealers regarding tissue MDA, GSH levels or serum parameters (p>0.05) at all time points examined. Both of the new root canal sealers showed good compatibility and acceptable tissue toxicity.

Protective effect of resveratrol against naphthalene-induced oxidative stress in mice.

OBJECTIVE: This investigation confirms the role of free radicals in naphthalene-induced toxicity and elucidates the mechanism of resveratrol (RVT). METHODS: Both male and female BALB-c mice were administered with naphthalene (100 mg/kg, i.p.) for 30 days, either along with saline or along with RVT (10mg/kg, orally). At the end of the experiment, following treatment and sacrifice of animals by decapitation, lung, liver and kidney tissue samples were taken for histological examination or determination of malondialdehyde (MDA), glutathione (GSH), myeloperoxidase (MPO) activity and collagen contents. Aspartate aminotransferase (AST), alanine aminotransferase (ALT), blood urea nitrogen (BUN) and creatinine levels and lactate dehydrogenase (LDH) activity were measured in the serum samples, while TNF-alpha, IL-beta, IL-6 and total antioxidant capacity (AOC) were assayed in plasma samples. RESULTS: Naphthalene administration caused a significant decrease in tissue GSH and plasma AOC, which was accompanied with significant increases in tissue MDA and collagen levels and MPO activity. Moreover, the pro-inflammatory mediators (TNF-alpha, IL-beta, IL-6), LDH activity, AST, ALT, creatinine and BUN levels were significantly increased in the naphthalene group. On the other hand, RVT treatment reversed all these biochemical indices as well as histopathological alterations induced by naphthalene. CONCLUSIONS: Oxidative mechanisms play an important role in naphthalene-induced tissue damage, and RVT, by inhibiting neutrophil infiltration, balancing oxidant-antioxidant status, and regulating the generation of inflammatory mediators, ameliorates oxidative organ injury due to naphthalene toxicity.

Melatonin protects against endosulfan-induced oxidative tissue damage in rats.

Endosulfan is a chlorinated cyclodiene insecticide which induces oxidative stress. In this study, we investigated the possible protective effect of melatonin, an antioxidant agent, against endosulfan (Endo)-induced toxicity in rats. Wistar albino rats (n = 8) were administered endosulfan (22 mg/kg/day orally) followed by either saline (Endo group) or melatonin (10 mg/kg/day, Endo + Mel group) for 5 days. In other rats, saline (control group) or melatonin (10 mg/kg/day, Mel group) was injected for 5 days, following corn oil administration (vehicle of endosulfan). Measurement of malondialdehyde (MDA) and glutathione (GSH) levels, myeloperoxidase (MPO) activity and collagen content were performed in liver and kidney. Furthermore, aspartate aminotransferase (AST), alanine aminotransferase (ALT), blood urea nitrogen (BUN), and creatinine levels, lactate dehydrogenase (LDH) activity were measured in the serum samples, while tumor necrosis factor-alpha (TNF-alpha), interleukin-beta (IL-beta) and total antioxidant capacity (AOC) were assayed in plasma samples. Endosulfan administration caused a significant decrease in tissue GSH and plasma AOC, which was accompanied with significant rises in tissue MDA and collagen levels and MPO activity. Moreover, the proinflammatory mediators (TNF-alpha and IL-beta), LDH activity, AST, ALT, creatinine and BUN levels were significantly elevated in the endosulfan-treated rats. On the other hand, melatonin treatment reversed all these biochemical alterations induced by endosulfan. Our results suggest that oxidative mechanisms play an important role in endosulfan-induced tissue damage and melatonin, by inhibiting neutrophil infiltration, balancing oxidant-antioxidant status and regulating the generation of inflammatory mediators, ameliorates oxidative organ injury as a result of endosulfan toxicity.

Nonprescription medication purchases and the role of pharmacists as healthcare workers in self-medication in Istanbul.

BACKGROUND: In Turkey, some drugs can be purchased from pharmacists without a prescription and there is no legal classification corresponding to the international term "over-the-counter drugs". The purpose of this study was to identify these non-prescribed drugs and to define the role of pharmacists in their sale and their use in primary healthcare. MATERIAL/METHODS: This cross-sectional study was carried out in Istanbul between December 1, 2003, and August 31, 2004. Seventy-three of the 901 pharmacies in two districts of Istanbul were chosen with systematic sampling, and information concerning drug sales and pharmacists' behavior regarding primary healthcare services was collected by observations as well as by interviews with the pharmacists. RESULTS: The study demonstrated that 41% of the drugs sold were non-prescribed. In pharmacies remote from healthcare institutions, remote from district centers, and in the summer seasons, the rates of non-prescribed drug sales were higher than those of prescribed drugs (Chi(2)=10.5, d.f.=1, p=0.001; Chi(2)=62.8, d.f.=1, p=0.0001; Chi(2)=23.4, d.f.=1, p=0.0001). The pharmacists stated that aside from drug sales, consumers visited them to consult about drugs, to get information on their health status, and to learn about family planning (78.1%, 72.1%, and 72.6% of the pharmacists, respectively). CONCLUSIONS: Extensive sale of non-prescribed drugs as a response to public demand, including those used for serious illnesses, has been observed in private pharmacies in Istanbul. The role of pharmacies and pharmacists in primary healthcare should be discussed more thoroughly and redefined on a legal basis.

Ginkgo biloba extract protects against mercury(II)-induced oxidative tissue damage in rats.

Mercury(II) is a highly toxic metal which induces oxidative stress in the body. In this study we aimed to investigate the possible protective effect of Ginkgo biloba (EGb), an antioxidant agent, against experimental mercury toxicity in rat model. Following a single dose of 5mg/kg mercuric chloride (HgCl(2); Hg group) either saline or EGb (150mg/kg) was administered for 5days. After decapitation of the rats trunk blood was obtained and the tissue samples from the brain, lung, liver, and kidney were taken for the determination of malondialdehyde (MDA) and glutathione (GSH) levels, myeloperoxidase (MPO) activity and collagen contents. Formation of reactive oxygen species in the tissue samples was monitored by chemiluminescence (CL) technique. BUN, creatinin, ALT, and AST levels and tumor necrosis factor-alpha (TNF-alpha) and lactate dehydrogenase (LDH) activity were assayed in serum samples. The results revealed that HgCl(2) induced oxidative damage caused significant decrease in GSH level, significant increase in MDA level, MPO activity and collagen content of the tissues. Treatment of rats with EGb significantly increased the GSH level and decreased the MDA level, MPO activity, and collagen contents. Similarly, serum ALT, AST and BUN levels, as well as LDH and TNF-alpha, were elevated in the Hg group as compared to control group. On the other hand, EGb treatment reversed all these biochemical indices. Our results implicate that mercury-induced oxidative damage in brain, lung, liver, and kidney tissues protected by G. biloba extract, with its antioxidant effects.

Ginkgo biloba extract reduces naphthalene-induced oxidative damage in mice.

This investigation elucidated the role of free radicals in naphthalene-induced toxicity and protection by Ginkgo biloba extract (EGb). BALB-c mice of either sex were administered with naphthalene (100 mg/kg; i.p.) for 30 days, along with either saline or EGb (150 mg/kg, orally). At the end of the experiment, following decapitation, lung, liver and kidney tissue samples were taken for histological examination or determination of malondialdehyde (MDA), glutathione (GSH), myeloperoxidase (MPO) activity and collagen contents. In addition, proinflammatory cytokines (TNF-alpha and IL-beta) and total antioxidant capacity (AOC) were assayed in the plasma, while lactate dehydrogenase (LDH) activity was assayed in serum samples. The results revealed that naphthalene caused a significant decrease in GSH level, and significant increases in MDA level, MPO activity and collagen content of tissues. Similarly, plasma cytokines, as well as serum LDH activity, were elevated while AOC was decreased in the naphthalene group compared with the control group. On the other hand, EGb treatment reversed all these biochemical indices. The results demonstrate that EGb extract, by balancing the oxidant-antioxidant status and inhibiting the generation of proinflammatory cytokines and neutrophil infiltration, protects against naphthalene-induced oxidative organ injury.

Protective effects of ginkgo biloba against acetaminophen-induced toxicity in mice.

BACKGROUND: The analgesic acetaminophen (AAP) causes a potentially fatal, hepatic centrilobular necrosis when taken in overdose. It was reported that these toxic effects of AAP are due to oxidative reactions that take place during its metabolism. OBJECTIVE: In this study, we aimed to investigate the possible beneficial effect of Ginkgo biloba (EGb), an antioxidant agent, against AAP toxicity in mice. METHODS: Balb/c mice were injected i.p. with: (1) vehicle, control (C) group; (2) a single dose of 50 mg/kg Ginkgo biloba extract, EGb group; (3) a single dose of 900 mg/kg i.p. acetaminophen, AAP group, and (4) EGb, in a dose of 50 mg/kg after AAP injection, AAP + EGb group. Serum ALT, AST, and tumor necrosis factor-alpha (TNF-alpha) levels in blood and glutathione (GSH), malondialdehyde (MDA) levels, myeloperoxidase (MPO) activity, and collagen contents in liver tissues were measured. Formation of reactive oxygen species in hepatic tissue samples was monitored by using chemiluminescence (CL) technique with luminol and lusigenin probe. Tissues were also examined microscopically. RESULTS: ALT, AST levels, and TNF-alpha were increased significantly (p < 0.001) after AAP treatment, and reduced with EGb. Acetaminophen caused a significant (p < 0.05-0.001) decrease in GSH levels while MDA levels and MPO activity were increased (p < 0.001) in liver tissues. These changes were reversed by EGb treatment. Furthermore, luminol and lusigenin CL levels in the AAP group increased dramatically compared to control and reduced by EGb treatment (p < 0.01). CONCLUSION: Our results implicate that AAP causes oxidative damage in hepatic tissues and Ginkgo biloba extract, by its antioxidant effects protects the tissues. Therefore, its therapeutic role as a "tissue injury-limiting agent" must be further elucidated in drug-induced oxidative damage.