Cadmium is known to be a carcinogenic metal that especially its compounds have sufficient evidence in both humans and experimental animals beneath its environmental effects. Testis tissue is highly sensitive to the effects of cadmium. It is proposed that cadmium also increases oxygen derived free radicals and lipid peroxidation. As indicators of oxidative DNA damage, 6 oxidative DNA bases were determined by using Gas Chromatography/Mass Spectrometry-Selected Ion Monitoring technique. 45 Sprague-Dawley rats (225-300 g) were used as experimental animals and were divided into 3 groups of 15 rats. A single 2 mg NaCl/kg body wt, 0,5 and 1,25 mg CdCl2/kg body wt were injected intraperitoneally to control, low and high dose groups, respectively. 5-OH Cytosine, 8-OH Adenine and Fapy Guanine lesions were elevated significantly in high dose group in the first day. A clear dose-response relationship was seen between dose groups and 8-OH Adenine levels related with time in all periods. There was a significant dose-response relationship in 2-OH Adenine, Fapy Guanine and 8-OH Guanine, especially in the second week suggesting the inhibition of XPA protein by cadmium after first week. In contrast, the observation of a significant decrease of 5-OH Cytosine levels after first week showed that cadmium could not affect the enzymes repairing the cytosine base lesions.
We suggest that TNFA (-238) variant may be a risk factor in both development and the severity of CWP, while TNFA (-308) variant seems to be important only in disease severity. On the other hand, IL6 variant may have a protective effect on the development and disease severity.
Paraoxonase (PON1) is a serum esterase responsible for the protection against xenobiotics toxicity such as paraoxon. Alterations in PON1 concentrations have been reported in a variety of diseases including diabetes mellitus (DM). It has been shown that the serum PON1 concentration and activity are decreased in patients with both type 1 and type 2 DM. This study aimed to investigate the lipid profiles and the relationship between PON1 activity and PON1, QR192 and LM55 polymorphisms in Turkish type 2 diabetic patients and non-diabetic control subjects. According to our results, RR variant had significantly higher PON activity than QQ and QR variants (p < 0.01) and LL variant had significantly higher PON activity than MM variant in both control and patient groups (p < 0.05). In conclusion, we found that PON1 192RR and 55LL genotypes are associated with higher PON activity than QQ and MM genotypes. This may be more protective to lipid peroxidation.
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