Prior exposure to restraint stress enhances 7,12-dimethylbenz(a)anthracene (DMBA) induced DNA damage in rats

Over the years, several lines of evidence have emerged supporting the role of stress in the development and progression of cancer. Stress can cause an increase in the production of reactive oxygen species (ROS) and decrease in the in vivo antioxidant defense systems. A ROS-induced DNA damage in peripheral lymphocytes, liver and skin cells may be revealed by Comet assay. To test whether DNA is damaged by stress/DMBA/stress and DMBA, rats were exposed to multiple doses of DMBA in the presence and absence of restraint stress, and DNA damage was evaluated. Insignificant differences were detected in all the three cells tested (peripheral lymphocytes, liver and skin cells) between control and stress treatment in terms of frequencies of damaged DNA. The extent of DNA migration was enhanced in DMBA treated rats in a dose dependent manner. Pre-stress DMBA treatment showed still higher frequencies of damage in comparison with control, stress alone or DMBA alone groups. Thus, prior exposure to stress clearly enhanced the DMBA induced DNA damage, especially so in the skin cells (target organ of the carcinogen application) than liver and peripheral lymphocytes as observed on the basis of the extent of DNA migration (tail DNA) during single cell gel electrophoresis.     

Biological and methodological implications of prostaglandin involvement in mouse brain lipid peroxidation measurements

Enhanced cyclooxygenase-mediated prostaglandin (PG) turnover occurring during sacrifice and biochemical processing of tissues also generates malondialdehyde (MDA), a product of lipid peroxidation (LPO). Studies reporting on LPO estimated by thiobarbituric acid reactive substances (TBARS) have failed to consider such artefactual increases. This study reports the relative proportion of PG metabolism-derived MDA (PG-MDA) in mouse brain regions during the TBARS assay. The cyclooxygenase inhibitor indomethacin significantly lowered MDA in fronto-parietal cortex and corpus striatum. Indomethacin (50–800 g/ml, in vitro) increased estimated TBARS in whole brain. Such enhancement was absent when indomethacin (20–80 g/sample) was added to the MDA standard curve, reflecting its interaction with TBARS other than MDA. PG-MDA contributes as much as 15% to the total estimated value of MDA in fronto-parietal cortex and corpus striatum and must be corrected for in LPO studies.     

Promotion by phosphate of Fe(III)- and Cu(II)-catalyzed autoxidation of fructose

Although the oxidative destruction of glucose and fructose has been studied by several investigators over the past century, the mechanism by which phosphate promotes these oxidation reactions is not known. A wide range of oxidation products have been used to monitor the oxidation of sugars and free radicals have been shown to be involved. The influence of phosphate concentration on the rate of production of free radicals and several sugar oxidation products has been studied. It was found that fructose is much more susceptible to autoxidation than glucose, galactose, or sucrose. The promotion of sugar oxidation by phosphate was found to be iron dependent. Addition of the iron chelators, diethylenetriaminepentaacetic acid (DTPA) and desferrioxamine completely suppressed the oxidation reactions, even at high concentrations of phosphate. Formaldehyde was positively identified as a product of fructose oxidation by HPLC analysis of its acetylacetone adduct. A mechanism is proposed in which phosphate cleaves the oxo bridges of the iron(III)-fructose complex, based on UV spectral analysis and magnetic susceptibility measurements, and thereby catalyzes the autoxidation of fructose.     

Ground and excited state proton transfer and antioxidant activity of 7-hydroxyflavone in model membranes: absorption and fluorescence spectroscopic studies

Steady state and time resolved fluorescence spectroscopy have been used to probe microenvironments of the therapeutically active intrinsically fluorescent flavonoid, 7-hydroxyflavone (7-HF), in model membranes consisting of multilamellar phosphatidylcholine liposomes. Additionally, the antioxidant effects of 7-HF against lipid peroxidation have been evaluated using spectrophotometric assay. Large Stokes shifted emissions with distinct spectroscopic signatures, are observed from the excited state proton transfer (ESPT) tautomer (which is generated by a solvent mediated mechanism) and the ground state anion of 7-HF. The neutral (7-HFN) and anionic (7-HFA) species' appear to be located in the non-polar acyl chain and the polar head group regions of the lipid vesicles respectively. The partition coefficients of 7-HFN and 7-HFA in these vesicles have also been estimated using their intrinsic fluorescence. Anisotropy (r) versus temperature (T) measurements reveal the utility of the tautomer fluorescence anisotropy as a sensitive parameter for exploring structural changes in the membranes. Fluorescence decay kinetics studies indicate heterogeneity in the microenvironments of both 7-HFN and 7-HFA. Furthermore, we demonstrate that lipid peroxidation of the model membranes is partially arrested upon 7-HF binding, suggesting its potential usefulness as an inhibitor of peroxidative damage of cell membranes.     

Type 1 ribosome-inactivating proteins—Entomotoxic, oxidative and genotoxic action on Anticarsia gemmatalis (Hübner) and Spodoptera frugiperda (J.E. Smith) (Lepidoptera: Noctuidae)

Ribosome-inactivating proteins (RIPs) from plants inhibit protein synthesis by inactivating ribosomes. Some two-chain (type 2) RIPs are highly toxic and may play a role in plant defense. The lower toxicity of single-chain (type 1) RIPs reflects the lack of a protein domain able to bind to, and translocate the toxin across cell membranes. We studied the effect of single-chain RIPs, lychnin, momordin, gelonin, PAP-S and saporin S-6, in larvae of Anticarsia gemmatalis and Spodoptera frugiperda. After ingesting a total dose of 20 or 40 μg of the toxins, weight gain, survival rate, lesions in DNA and oxidative status (catalase and superoxide dismutase activities and lipidic peroxidation) of RIP-treated insects were assayed. Momordin was the less toxic in the biossays. S. frugiperda had a more pronounced weight loss on the 4th day of treatment and A. gemmatalis on the 10th day. RIP-induced mortality reached 57.13% for A. gemmatalis and 29.45% for S. frugiperda. RIP-treated insects showed a 2-3-fold increase in DNA lesions as assessed by the comet assay, but there were no correlations between stress markers and DNA damage. We conclude that single-chain RIPs are entomotoxic to lepidopteran insects causing extensive DNA lesions.     

Protective effect of fosfomycin on gentamicin-induced lipid peroxidation of rat renal tissue

Fosfomycin is clinically recognized to reduce the aminoglycoside antibiotics-induced nephrotoxicity. However, little has been clarified why fosfomycin protects the kidney from the aminoglycosides-induced nephrotoxicity. Gentamicin, a typical aminoglycoside, is reported to cause lipid peroxidation. We focused on lipid peroxidation induced by gentamicin as a mechanism for the aminoglycosides-induced nephrotoxicity. The aim of this study is to investigate the effect of fosfomycin on the gentamicin-induced lipid peroxidation. In rat renal cortex mitochondria, fosfomycin was shown to depress the gentamicin-induced lipid peroxidation, which was evaluated by formation of thiobarbituric acid reactive substances (TBARS). Interestingly, this effect was observed in rat renal cortex mitochondria, but not in rat liver microsomes. However, fosfomycin did not affect lipid peroxidation of arachidonic acid caused by gentamicin with iron. Fosfomycin inhibited the gentamicin-induced iron release from rat renal cortex mitochondria. These results indicated that fosfomycin inhibited the gentamicin-induced lipid peroxidation by depressing the iron release from mitochondria. This may possibly be one mechanism for the protection of fosfomycin against the gentamicin-induced nephrotoxicity.     

Effect of chromium(VI) on the status of plasma lipid peroxidation and erythrocyte antioxidant enzymes in chromium plating workers

OBJECTIVES: The present study was carried out to determine the effect of chromium(VI) on the status of plasma lipid peroxidation and erythrocyte antioxidant enzymes in workers exposed to chromium during chromium plating process. METHODS: Fifty subjects working in chromium plating process formed the study group. An equal number of age-sex matched subjects working in administrative units formed the control group. The control subjects were residing in the same city but away from the work place of study group subjects. Urinary chromium levels were determined by using a graphite furnace atomic absorption spectrophotometer. The plasma lipid peroxidation and erythrocyte antioxidant enzymes were determined by using spectrophotmetric methods. RESULTS: A significant increase of plasma lipid peroxidation and a significant decrease of superoxide dismutase and glutathione peroxidase levels were noted in the study group as compared with the controls. The level of plasma lipid peroxidation was positively and erythrocyte antioxidant enzymes were negatively and significantly correlated with chromium levels in urine. Multiple regression analysis was assessed the oxidative stress associated with chromium and life style confounding factors such as BMI, coffee, tea, alcohol and smoking. The multiple regression analysis showed that the urine chromium levels >10 micro g/g of creatinine, smoking, consumption of green vegetables and BMI variables were significantly associated with the levels of oxidative stress. CONCLUSION: The results show that the increased plasma lipid peroxidation and decreased antioxidant enzymes (superoxide dismutase and glutathione peroxidase) observed in chromium-exposed workers could be used as biomarkers of oxidative stress.     

Bacopa monnieri modulates endogenous cytoplasmic and mitochondrial oxidative markers in prepubertal mice brain

Bacopa monnieri (BM) an herb, found throughout the Indian subcontinent in wet, damp and marshy areas is used in Ayurvedic system of medicine for improving intellect/memory, treatment of anxiety and neuropharmacological disorders. Although extensively given to children as a memory enhancer, no data exists on its ability to modulate neuronal oxidative stress in prepubertal animal models. Hence in this study, we examined if dietary intake of BM leaf powder has the propensity to modulate endogenous markers of oxidative stress, redox status (reduced GSH, thiol status), response of antioxidant defenses (enzymic), protein oxidation and cholinergic function in various brain regions of prepubertal (PP) mice. PP mice maintained on a BM-enriched diet (0.5 and 1%) for 4 weeks showed a significant diminution of basal oxidative markers (malondialdehyde levels, reactive species generation, hydroperoxide levels and protein carbonyls) in both cytoplasm and mitochondria of all brain regions. This was accompanied with enhanced reduced glutathione, thiol levels and elevated activities of antioxidant enzymes (catalase, glutathione peroxidase, superoxide dismutase). Significant reduction in the activity of acetyl cholinesterase enzyme in all brain regions suggested the potential of BM leaf powder to modulate cholinergic function. Further evidence that dietary intake of BM leaf powder confers the prepubertal brain with additional capacity to cope up with neurotoxic prooxidants was obtained by exposing cortical/cerebellar synaptosomes of normal and BM fed mice to 3-nitropropionic acid (3-NPA). While synaptosomes from control mice exhibited a concentration related lipid peroxidation and ROS generation, synaptosomes obtained from BM fed mice showed only a marginal induction at the highest concentration clearly suggesting their increased resistance to 3-NPA-induced oxidative stress. Collectively these data clearly indicate the potential of Bacopa monnieri to modulate endogenous markers of oxidative stress in brain tissue of PP mice. Based on these results, it is hypothesized that dietary intake of BM leaf powder confers neuroprotective advantage and is likely to be effective as a prophylactic/therapeutic agent for neurodegenerative disorders involving oxidative stress.     

Induction of apoptosis in K562/ADM cells by gamma-linolenic acid involves lipid peroxidation and activation of caspase-3

Numerous studies have revealed that gamma-linolenic acid (GLA) possesses effective tumoricidal properties while not inducing damage to normal cells or creating harmful systemic side effects. It can exert anti-tumor efficacy against a variety of cancers including leukemia. However, little is known about the effects of GLA on leukemia resistant to chemotherapy, emerging as a serious clinical problem. The present study tested GLA-induced apoptosis in K562/ADM multidrug-resistant (MDR) leukemic cells and investigated its possible mechanisms. Using cell viability, fluorescent staining of nuclei, flow cytometric Annexin V/PI double staining and lactate dehydrogenase (LDH) release, we found that GLA could inhibit cell growth and induce apoptosis and secondary necrosis. The results showed that incubation with GLA concentrations of 10-60 microg/ml caused a dose- and time-dependent decrease of K562/ADM cell viability, and the IC50 value was 50.5 microg/ml at 24 h and 31.5 microg/ml at 48 h. Flow cytometry using Annexin V/PI double staining assessed apoptosis, necrosis and viability. Typical apoptotic nuclei were shown by staining of K562/ADM cells with DNA-binding fluorochrome Hoechst 33342, characterized by chromatin condensation and nuclear fragmentation. On the other hand, after treated K562/ADM cells with 20 microg/ml GLA for 48 h and with 40 microg/ml GLA for 12 h, the LDH release significantly increased, indicated losses of plasma membrane integrity and presence of necrosis. Further, the inhibition of GLA-induced apoptosis by a pan-caspase inhibitor (z-VAD-fmk) suggested the involvement of caspases. The increase of caspase-3 activity with GLA concentration confirmed its role in the process. The results also showed that the malondialdehyde (MDA) content was also significantly elevated, and antioxidant BHT could block GLA cytotoxity, indicating the cytotoxity induced by GLA may be due to lipid peroxidation.     

Fasciola hepatica: effects on the antioxidative properties and lipid peroxidation of rat serum

Fasciola hepatica infection is accompanied by increased formation of reactive oxygen species. The aim of this study was to analyze antioxidative properties of rat serum in the course of fasciolosis. Wistar rats were infected per os with 30 metacercariae of F. hepatica. Activities of antioxidant enzymes and concentrations of non-enzymatic antioxidants in serum were determined at 4, 7, and 10 weeks post-infection (wpi). Activity of superoxide dismutase (Cu, Zn-SOD) significantly decreased (by 35% during the migratory phase, by 40 and 23% at 7 and 10 wpi, respectively), while glutathione reductase activity significantly increased (by 62, 65, and 41%, at 4, 7, and 10 wpi, respectively). No significant changes were found in the activity of glutathione peroxidase. Significant decreases in concentrations of reduced glutathione, vitamins C, E, and A were observed, particularly during the migratory phase of fasciolosis (at 4 wpi). These changes were accompanied by enhancement of lipid peroxidation processes as evidenced by increased levels of malondialdehyde (MDA) and 4-hydroxynonenal (4-HNE). Concentrations of MDA and 4-HNE at 4 wpi increased by 38% and by 59%. MDA increased by 51% at 7 wpi and by 79% at 10 wpi, while 4-HNE increased by 87 and 118%, respectively. The results indicate that fasciolosis is associated with enhanced oxidative reactions and reduced antioxidant defense capability of rat serum.     

Naproxen-induced oxidative stress in the isolated perfused rat liver

We previously showed that naproxen induced the oxidative stress in the liver microsomes and the isolated hepatocytes of rats. In this study, the in situ effect of naproxen on the rat liver tissue was investigated, using the isolated perfused liver from the view-point of the naproxen-induced hepatotoxicity. The leakage of glutamic-oxaloacetic transaminase (GOT) from the perfused liver and appearance of thiobarbituric acid reactive substances (TBARS) in the perfusate increased with the progress of perfusion after a lag time of about 1h. The naproxen-perfusion of the liver decreased the biliary excretion of glutathione (GSH) and oxidized glutathione, glutathione disulfide (GSSG) prior to TBARS production and GOT leakage. GSSG content in the naproxen-perfused liver was significantly higher than in the control. TBARS appeared in the perfusate of the naproxen-perfused liver for 30 min, but not in the control. The biliary excretion clearance (CL(bile)) of indocyanine green (ICG), a reagent for testing the liver function, in the liver perfused with naproxen decreased to a half of that in the liver perfused without naproxen. Thus, the naproxen-induced oxidative stress in the liver was shown to affect the physiological function of liver through the impairment of biliary excretion, which is recognized as a detoxification system.     

Phosphorus deficiency enhances aluminum tolerance of rice (Oryza sativa) by changing the physicochemical characteristics of root plasma membranes and cell walls

The negative charge at the root surface is mainly derived from the phosphate group of phospholipids in plasma membranes (PMs) and the carboxyl group of pectins in cell walls, which are usually neutralized by calcium (Ca) ions contributing to maintain the root integrity. The major toxic effect of aluminum (Al) in plants is the inhibition of root elongation due to Al binding tightly to these negative sites in exchange for Ca. Because phospholipid and pectin concentrations decrease in roots of some plant species under phosphorus (P)-limiting conditions, we hypothesized that rice (Oryza sativa L.) seedlings grown under P-limiting conditions would demonstrate enhanced Al tolerance because of their fewer sites on their roots. For pretreatment, rice seedlings were grown in a culture solution with (+P) or without (−P) P. Thereafter, the seedlings were transferred to a solution with or without Al, and the lipid, pectin, hemicellulose, and mineral concentrations as well as Al tolerance were then determined. Furthermore, the low-Ca tolerance of P-pretreated seedlings was investigated under different pH conditions. The concentrations of phospholipids and pectins in the roots of rice receiving −P pretreatment were lower than those receiving +P pretreatment. As expected, seedlings receiving the −P pretreatment showed enhanced Al tolerance, accompanied by the decrease in Al accumulation in their roots and shoots. This low P-induced enhanced Al tolerance was not explained by enhanced antioxidant activities or organic acid secretion from roots but by the decrease in phospholipid and pectin concentrations in the roots. In addition, low-Ca tolerance of the roots was enhanced by the −P pretreatment under low pH conditions. This low P-induced enhancement of low-Ca tolerance may be related to the lower Ca requirement to maintain PM and cell wall structures in roots of rice with fewer phospholipids and pectins.     

Free radical scavenging activity of the Japanese herbal medicine Toki-Shakuyaku-San (TJ-23) and its effect on superoxide dismutase activity,lipid peroxides,glutamate, and monoamine metabolites in aged rat brain

The free radical scavenging activity of the Japanese herbal medicine, Toki-Shakuyaku-San (TJ-23; TSUMURA & Co., Tokyo, Japan), was examined using electron spin resonance (ESR) spectrometry. TJ-23 scavenged 1,1-diphenyl-2-picrylhydrazyl radicals (DPPH), superoxide (O₂ ⁻), and hydroxyl radicals (·OH) dose-dependently. It also diminished carbon centered radicals (·C) generated by oxidative stress and inhibited thiobarbituric acid-reactive substances (TBARS) formation in mouse cortex homogenate. In addition, the effect of TJ-23 on the concentration of neurotransmitters and TBARS formation, and superoxide dismutase (SOD) activity in the cortex, hippocampus and striatum of the aged rat brain was studied. The concentrations of the metabolites of monoamines, glutamate and glutamine were decreased by 4 weeks of oral administration of TJ-23. The SOD activity of mitochondrial fraction was increased and TBARS formation was significantly suppressed. These results suggest that TJ-23 has an antioxidant action and would have a prophylactic effect against free radical-mediated neurological diseases associated with aging.     

Ecotoxocological effects of short-term exposure to a human pharmaceutical Verapamil in juvenile rainbow trout (Oncorhynchus mykiss)

Verapamil (VRP) is a calcium channel blocker that is a highly prescribed compound and commonly present in aquatic environment, but the ecotoxicological effects of this pharmaceutical in fish have not been fully documented. In this study, the toxic effects of VRP were studied in juvenile rainbow trout, Oncorhynchus mykiss, by acute static bioassay. In the acute test, the median lethal concentration (LC50, 2.72 mg/L) was evaluated and the behavioral changes were obviously intensified with increasing VRP concentrations. Compared to the control, oxidative stress was observed in fish tissues with different levels after short-term exposure to sublethal concentrations (0.27 and 1.35 mg/L) of VRP. Activities of SOD and GPx in fish brain were induced at 0.27 mg/L VRP, but all the antioxidant enzymes (SOD, GPx and GR) in fish brain were decreased at 1.35 mg/L VRP. When compared to the control, all the antioxidant enzymes in gill were decreased in both treated groups, but there was no significant change in muscle. Additional, muscle DNA/RNA ratio in fish exposed at 1.35 mg/L VRP was significantly lower than that in the control. Furthermore, through chemometrics of all parameters measured in fish exposed to sublethal VRP concentrations using principal component analysis, two groups with 89.8% of total accumulated variance were distinguished. In short, the physiological and biochemical responses in of fish indicated that VRP-induced environmental stress; but according to VRP residual status in the natural environment, more long-term experiments at lower concentrations will be necessary in the future.     

In vitro effects of bisphenol A on the quality parameters,oxidative stress,DNA integrity and adenosine triphosphate content in sterlet (Acipenser ruthenus) spermatozoa

Among endocrine disruptors, the xenoestrogen bisphenol A (BPA) deserves particular attention due to widespread human exposure. Besides hormonal effects, BPA has been suspected to be responsible for adverse effect on reproductive ability of various species. In the present study the effect of BPA on the quality parameters, oxidative stress, the DNA integrity and intracellular ATP content of sterlet (Acipenser ruthenus) spermatozoa were investigated in vitro. Fish spermatozoa were exposed to concentrations of BPA possibly occurring in nature (0.5, 1.75, 2.5, 5 and 10 μg/L) for 2 h. Results revealed that BPA significantly decreased spermatozoa motility and velocity of spermatozoa at concentration of BPA 2.5–10 μg/L. Significant positive correlation (r = 0.713, P < 0.05) was found between percent motile spermatozoa and ATP content. Oxidative stress was observed at concentrations 1.75–10 μg/L, as reflected by significantly higher levels of protein and lipid oxidation and superoxide dismutase activity. Intracellular ATP content of spermatozoa decreased with increasing concentrations of BPA. A dramatic increase in DNA fragmentation expressed as percent tail DNA (2.2% ± 0.46) and Olive tail moment (0.37 ± 0.09 arbitrary units) was recorded at concentrations of 1.75 μg/L and above. The present study confirms that concentrations of BPA that can be encountered in nature are capable to induce oxidative stress, leading to impaired sperm quality, DNA fragmentation and intracellular ATP content.     

Effects of subacute treatment of ethylene glycol on serum marker enzymes and erythrocyte and tissue antioxidant defense systems and lipid peroxidation in rats

The present study was aimed to investigate the effects of ethylene glycol (EG) on serum marker enzymes, antioxidant defense systems and lipid peroxidation concentration (malondialdehyde=MDA) in various tissues of rats exposed to ethylene glycol. EG (1.25% or 2.5%) in drinking water was administered orally to rats (Sprague-Dawley albino) ad libitum for 21 days continuously. EG treatments caused different effects on the serum marker enzymes, antioxidant defense system and MDA content in various tissues of the treatment groups as compared with the controls. EG also caused a significant increase in the serum marker enzyme activities with 2.5% dosage whereas, no changes were not observed with 1.25% dosage of EG treatment. Lipid peroxidation significantly increased in all the tissues except for in the heart and stomach of rats treated with both dosages of EG. Also, the antioxidative systems were also seriously affected by EG. For example, SOD significantly decreased in the liver treated with both dosages whereas, SOD activity in the erythrocytes, kidney, heart and stomach were significantly increased and not changed in the brain with two dosages of EG. Also, while CAT activity significantly decreased in the erythrocytes, liver and kidney, the activity in the stomach significantly increased, but did not change in the brain and heart with two doses of EG. GR activity significantly decreased in the erythrocytes treated with both dosages of EG whereas GR was not affected in other tissues by EG treatment. GST activity significantly elevated in the heart and brain but did not change in the other tissues of rats treated with both dosages of EG. Meanwhile, GSH depletion in the erythrocytes of rats treated with 2.5% dosage of EG was found to be significant whereas, the level of GSH in the brain was significantly increased treated with both the dosages of EG. The observations presented led us to conclude that the administration of subacute EG promotes lipid peroxidatin content, elevates tissue damage serum marker enzymes and changes in the antioxidative systems in rats. These data, along with the determined changes suggest that EG produced substantial systemic organ toxicity in the erythrocyte, liver, brain, heart kidney and stomach during the period of a 21-day subacute exposure.     

Melatonin and structural analogues do not possess antioxidant properties on Fe(2+)-initiated peroxidation of sonicated liposomes made of retinal lipids

Melatonin and its structural analogues display antioxidant activity in vivo but their activity in model membranes is not very well known. In this study, we have investigated the antioxidant capacity of melatonin and structural analogues on Fe²⁺-initiated peroxidation of sonicated liposomes made of retinal lipids. The indoleamines were evaluated against butylated hydroxitoluene (BHT) which was chosen as a reference standard because of its high antioxidant capacity. After the addition of Fe²⁺ as initiator of lipid peroxidation, quick production of conjugated dienes was observed. With addition of increasing concentrations of BHT the start of the reaction was delayed and initial reaction rates were lower. However, this reduction was not proportional to the increase in concentration. The start of the reaction and initial reaction rates were not modified in the presence of melatonin and its structural analogues. The formation of TBARS started immediately after the addition of Fe²⁺. The increase in the concentration of BHT avoided the emergence of TBARS. Changes were not observed in the presence of melatonin or structural analogues. Retinal lipids showed a high content of docosahexaenoic (22: 6 ^{Δ4,7,10,13,16,19}) acid, characteristic of this tissue. A little bit of that fatty acid was lost when sonicated liposomes were prepared with these retinal lipids. The polyunsaturated fatty acids (PUFAs) diminished significantly after incubation of liposomes with Fe²⁺ during 1 h. BHT preserved PUFAs whereas melatonin and its related indoleamines did not. These data reinforce the hypothesis that melatonin and structural analogues do not possess antioxidant properties per se in this liposomal model system.     

Growth promotion and a decrease of oxidative stress in maize seedlings by a combination of geomagnetic and weak electromagnetic fields

In the present study, we hypothesized that an appropriate combination of a geomagnetic field (as a static field) and an alternative magnetic field may result in the promotion of maize seedling growth by an alleviation of an excess production of reactive oxygen species. First, we determined the applicable range of frequencies by theoretical calculations, and a combined magnetic field was designed. The seeds were germinated in the magnetic field for 4 days, and the seedlings were allowed to grow in a nutrient solution for another 4 days. The magnetic field-treated maize seeds produced seedlings with a faster growth rate than the control seeds. The activity of superoxide dismutase in the magnetic field-treated seedlings was lower, while the total antioxidant capacity of these seedlings was higher than that of the control group. The maintenance of membrane integrity and a decrease of iron content in the magnetic field-treated seedlings suggest that a combination of both static and alternative magnetic fields promotes the growth of the plants by lowering iron absorption, a reduction in the Fenton chemistry, and lowering the risk of oxidative burst.