Background. Microwaves from mobile phones are one of the environmental toxicants that are capable of compromising male fertility by inducing oxidative stress and apoptosis in the testes. Melatonin is a lipophilic tryptophan indole amine and a potent antioxidant. Objectives. The aim of the study was to evaluate the effect of melatonin treatment on oxidative stress parameters and DNA fragmentation in the testicular tissue of rats exposed to microwave radiation (4 h/day). Material and Methods. Adult Wistar rats were divided in 4 groups: I -treated with saline; II -treated with melatonin; III -exposed to microwaves; IV -exposed to microwaves and treated with melatonin. The melatonin (2 mg/kg ip) was administered daily. The animals were sacrificed after 20, 40 and 60 days. Results. Melatonin treatment prevented previously registered increases in malondialdehyde after only 20 days. Furthermore, it reversed the effects of microwave exposure on xanthine oxidase (after 40 days) and acid-DNase activity (after 20 days). However, neither protein carbonyl content nor catalase and alkaline Dnase activity were changed due to melatonin treatment. Conclusions. Melatonin exerts potent antioxidant effects in the testes of rats exposed to microwaves by decreasing the intensity of oxidative stress; it also reduces DNA fragmentation (Adv Clin Exp Med 2015, 24, 3, 429-436).

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Accumulation of hydrophobic bile acids (BAs) during cholestasis plays an important role in apoptosis initiation as well as oxidative stress increase in liver cells. Ursodeoxycholic acid (UDCA) acts as a protector in BA-induced cell injury.The aim of the study was to evaluate the effect of UDCA on oxidative stress level and DNase I and II activity caused by liver injury in bile duct ligation (BDL) rats.Wistar rats were divided in four groups: group 1, control (sham-operated); group 2, sham-operated and injected with UDCA (30 mg/kg); group 3,animals with BDL; and group 4,UDCA-treatedcholestatic rats. Animals were sacrificed after 9 days. Malondialdehyde (MDA; lipid peroxidation end-product) level and protein-molecule oxidative modification (carbonyl group content) significantly increased in BDL rat liver. Catalase (CAT) activity in liver tissue was found to be decreased in BDL rats. In addition, xanthine oxidase (XO) activity, which is thought to be one of the key enzymes producing reactive oxygen species, was found to be increased in the cholestatic group. The apoptotic effect in cholestasis was probably triggered by the increased activation of DNase I and II. The protective effect of UDCA on liver tissue damage in BDL rats, in comparison to cholestatic liver, were 1) decrease of MDA levels, 2) increased CAT activity, 3) reduced XO activity, and 4) effect on terminal apoptotic reaction, shown as a decrease in DNase I and II activity.Therefore, UDCA may be useful in the preservation of liver function in cholestasis treatment.

Abstract:Objectives: We aimed to clarify if melatonin treatment (2 mg/kg i.p.) may favorably impact the liver tissue in rats exposed to microwave radiation. The experiment was performed on 84 six-weeks-old Wistar male rats exposed for 4h a day, for 20, 40 and 60 days, respectively, to microwaves (900 MHz, 100-300 microT, 54-160 V/m). Rats were divided in to four groups: I (control) -rats treated with saline, II (Mel) -rats treated with melatonin, III (MWs) -microwave exposed rats, IV (MWs + Mel) -MWs exposed rats treated with melatonin. We evaluated oxidative stress parameters (malondialdehyde and carbonyl group content), catalase, xanthine oxidase, deoxyribonuclease I and II activity. Background: Oxidative stress is the key mechanism of the microwave induced tissue injury. Melatonin, a lipophilic indoleamine primarily synthesized and released from the pineal gland is a powerful antioxidant. Results: Exposure to microwaves caused an increase in malondialdehyde after 40 (p < 0.01), protein carbonyl content after 20 (p < 0.05), catalase (p < 0.05) and xantine oxidase activity (p < 0.05) after 40 days. Increase in deoxyribonuclease I activity was observed after 60 days (p < 0.05), while deoxyribonuclease II activity was unaffected. Melatonin treatment led to malondialdehyde decrease after 40 days (p< 0.05), but surprisingly had no effect on other analyzed parameters. Conclusion: Melatonin exerts certain antioxidant effects in the liver of rats exposed to microwaves, by diminishing the intensity of lipid peroxidation (Fig. 6, Ref. 32).Text in PDF www.elis.sk.

Hepatitis C virus (HCV) is a major cause of liver disease worldwide. Chronic HCV infections are usually associated with increased oxidative stress in the liver tissue. The intensity of oxidative stress may be a detrimental factor in liver injury and may determine the severity of the disease. The aim of the present case-control study was to determine the level of lipid peroxidation (TBARS), protein oxidative modification (AOPP), and catalase activity in sera of patients infected with HCV, in relation to different HCV genotypes and viral load. Considering the HCV patients with chronic hepatitis C (52) and control subject (50) recruitment, the study was designed as a case–control-type. The HCV RNA isolation, viral load, and HCV genotyping were performed according to the standard protocols. A significant difference compared to control healthy subjects was reported for TBAR ( p < 0.001 ), AOPP ( p = 0.001 ), and catalase activity ( p = 0.007 ). In a gender-based comparison, a significantly higher level of AOPP for females was reported ( p < 0.001 ). As stratified by HCV genotype, the most common was HCV-1 (HCV-1a and HCV 1b), with the overall participation of more than 60%, followed by genotype 3, while the least represented was genotype 2. No significant difference was documented among genotypes in regard to oxidative stress markers, although somewhat higher TBARS level, but not significant, was registered in patients infected with genotype 1b. A statistically significant positive correlation was found between the concentration of HCV genome copies and AOPP ( r = 0.344 ; p = 0.012 ). A high level of HCV viral load was more likely to have a higher TBARS, but still without statistical significance ( p = 0.072 ). In conclusion, the results obtained confirmed an imbalance between the ROS production and antioxidative defense system in HCV-infected patients. Since oxidative stress may have a profound influence on disease progression, fibrosis, and carcinogenesis, our results may meet the aspirations of mandatory introduction of antioxidants as early HCV therapy to counteract ROS consequences.

This study examined the hepatoprotective and anti-inflammatory effects of anthocyanins from Vaccinim myrtillus (bilberry) fruit extract on the acute liver failure caused by carbon tetrachloride-CCl4 (3 mL/kg, i.p.). The preventive treatment of the bilberry extract (200 mg anthocyanins/kg, orally, 7 days) prior to the exposure to the CCl4 resulted in an evident decrease in markers of liver damage (glutamate dehydrogenase, sorbitol dehydrogenase, malate dehydrogenase), and reduced pro-oxidative (conjugated dienes, lipid hydroperoxide, thiobarbituric acid reactive substances, advanced oxidation protein products, NADPH oxidase, hydrogen peroxide, oxidized glutathione), and pro-inflammatory markers (tumor necrosis factor-alpha, interleukin-6, nitrite, myeloperoxidase, inducible nitric oxide synthase, cyclooxygenase-2, CD68, lipocalin-2), and also caused a significant decrease in the dissipation of the liver antioxidative defence capacities (reduced glutathione, glutathione S-transferase, and quinone reductase) in comparison to the results detected in the animals treated with CCl4 exclusively. The administration of the anthocyanins prevented the arginine metabolism’s diversion towards the citrulline, decreased the catabolism of polyamines (the activity of putrescine oxidase and spermine oxidase), and significantly reduced the excessive activation and hyperplasia of the Kupffer cells. There was also an absence of necrosis, in regard to the toxic effect of CCl4 alone. The hepatoprotective mechanisms of bilberry extract are based on the inhibition of pro-oxidative mediators, strong anti-inflammatory properties, inducing of hepatic phase II antioxidant enzymes (glutathione S-transferase, quinone reductase) and reduced glutathione, hypoplasia of Kupffer cells, and a decrease in the catabolism of polyamines.

The nature of an electromagnetic fi eld is not the same outside and inside a biological subject. Numerical bioelectromagnetic simulation methods for penetrating electromagnetic fi elds facilitate the calculation of fi eld components in biological entities. Calculating energy absorbed from known sources, such as mobile phones when placed near the head, is a prerequisite for studying the biological infl uence of an electromagnetic fi eld. Such research requires approximate anatomical models which are used to calculate the fi eld components and absorbed energy. In order to explore the biological effects in organs and tissues, it is necessary to establish a relationship between an analogous anatomical model and the real structure. We propose a new approach in exploring biological effects through combining two different techniques: 1) numerical electromagnetic simulation, which is used to calculate the fi eld components in a similar anatomical model and 2) Magnetic Resonance Imaging (MRI), which is used to accurately locate sites with increased absorption. By overlapping images obtained by both methods, we can precisely locate the spots with maximum absorption effects. This way, we can detect the site where the most pronounced biological effects are to be expected. This novel approach successfully overcomes the standard limitations of working with analogous anatomical models. Arh Hig Rada Toksikol 2013;64:159-168 KEY WORDS: accurate locating, computational bioelectromagnetic modelling, electromagnetic fi eld, specifi c absorption rate (SAR) Krstić et al. PREDICTING BIOLOGICAL EFFECTS OF MOBILE PHONE RADIATION

AIM: Carbon tetrachloride (CCl 4) is an organic chemical that produces different tissue-damaging effects when ingested or inhaled. Present study aims to determine whether the application of exogenous melatonin, a neurohormone with numerous biological properties, can prevent disturbances in lung tissue antioxidative capacities and arginine metabolism, tissue infl ammation and oxidative damage induced by exposure to CCl 4 in rats. METHODS: The effects of melatonin on the changes occurring in rat lung tissue after an acute exposure to CCl 4 were studied by monitoring alterations in antioxidant capacities, infl ammatory parameters, parameters of arginine metabolism, and lipid and protein oxidative damage. RESULTS: The results indicated that melatonin prevents CCl 4-induced lung damage by mitigating tissue antioxidant capacity and preventing nitric oxide production through a shift from nitric oxide synthase to arginase. Also, melatonin partially prevented tissue infl ammation and molecules' oxidative modifi cation seen after exposure to CCl 4. CONCLUSIONS: The protective activity of melatonin can be attributed to its ability to scavenge both free radicals, as well as to its potential to increase tissue antioxidant capacity. The modulation of infl ammatory response through both decrease in tissue infl ammatory parameters and infl uence on arginine-nitric oxide metabolism might be an additional mechanism of action (Tab. 1, Fig. 2, Ref. 33).