Assessment of DNA damage and plasma catalase activity in healthy term hyperbilirubinemic infants receiving phototherapy.

Phototherapy (PT) is the most widely used form of treatment for unconjugated hyperbilirubinemia. One possible harmful consequence of PT is of a genetic nature. High levels of bilirubin may lead to oxidative damage in newborns: photochemical reactions may produce toxic photoproducts, probably peroxides. In order to investigate this hypothesis further under in vivo conditions, DNA strand-break frequency was examined by means of the comet assay in peripheral lymphocytes of icteric newborns undergoing PT treatment, and the levels of catalase, an antioxidant enzyme, were determined. We analyzed 20 term non-hemolitic hyperbilirubinemic jaundiced neonates before PT ('before PT' group) and just prior to ending PT ('after PT' group) and compared comet scores of these patients with those of 20 healthy term neonates who all had bilirubin levels in the physiological range. Comet scores (tail length, tail moment and %DNA in tail) of the group 'before phototherapy' were 23.5 +/- 16.3, 7.41 (0.97-40.7), 33.0 +/- 12.1, respectively and scores of after phototherapy group were 3.2 +/- 1.8, 0.29 (0.3-3.2), 10.7 +/- 3.7, respectively. Comet scores of the control group were 3.0 +/- 2.9, 0.25 (0.03-3.22), 10.9 +/- 4.5, respectively. Comet scores and plasma catalase activities in hyperbilirubinemic newborns were significantly higher before phototherapy, compared with the values after phototherapy and in the control groups (p < 0.001). There was no statistical difference between the 'after phototherapy' group and the controls (p > 0.05). These results indicate that high serum bilirubin level has genotoxic effects as is evident from the high rate of DNA strand-breaks in jaundiced newborns. Also PT does not cause an increase in DNA oxidation or induce the genotoxic effects of bilirubin. The counteracting effect of higher catalase activities in hyperbilirubinemic newborns may be responsible for the inactivating toxic and DNA-damaging effects of PT.

Serum zinc level and its effect on anthropometric measurements in 7-11 year-old children with different socioeconomic backgrounds.

This study was performed in order to determine the serum zinc (Zn) level of primary school students, to show the effect of socioeconomic status (SES) on the zinc level, and finally to show the effect of zinc deficiency on the anthropometric parameters. Ten different primary schools were included in the study according to SES. Four-mL venous blood samples were obtained under fasting conditions using disposable plastic syringes. Four hundred thirty-two randomly chosen students between 7 and 11 years of age were investigated. All the children were living in Sivas, a city located in the middle eastern part of Turkey. Serum Zn level was measured by atomic absorption spectrophotometry (Hitachi 2-800). The weight and height of each child was recorded. The SES of children included in this study was as follows: 43.1% low (n = 186), 34.3% middle (n = 148), and 22.7% high (n = 98). Mean serum Zn levels of low and middle SES subjects were 56.3 +/- 17.50 micrograms/dL and 86.6 +/- 26.8 micrograms/dL respectively, while in children with high SES the mean serum Zn was 110.7 +/- 24.50 micrograms/dL. The difference between the groups was found to be statistically significant (F = 19.545, p < 0.05). When height-for-age z-scores were calculated according to SES, 105 of 186 children (56.4%) with low SES were found to have a z-score of -2 or lower and 14 of 147 children with middle SES had a z-score of -2 or lower. None of the children in the high SES group had a z-score of -2 or lower.

Investigation of protein oxidation and lipid peroxidation in patients with rheumatoid arthritis.

We aimed to determine the importance of neutrophil activation and the source of oxidative stress in the pathogenesis of rheumatoid arthritis (RA) by quantification of advanced oxidation protein products (AOPP) and total thiol levels as markers of oxidative protein damage, malondialdehyde (MDA) levels as a marker of lipid peroxidation and myeloperoxidase (MPO) activity as a marker of neutrophil activation in patients with RA. Fifty-seven rheumatoid arthritis patients were included in the study and sub-grouped according to disease activity (active, n = 31; inactive, n = 26) and compared with healthy controls (n = 25). Serum MPO activity, AOPP, MDA, and thiol levels were measured by an enzymic spectrophotometric method. Serum MPO activity (p < 0.001), AOPP (p < 0.001), MDA (p < 0.001) and levels of thiol (p < 0.002), were higher in the patient group than the controls. Active and inactive RA groups were compared with the control group and there were significant differences between each parameter. MPO activity, AOPP, MDA and thiol levels were significantly higher in both active and inactive RA patients than the controls. On the other hand, when a comparison was made between active and the inactive stage, a statistically significant difference was present only in MDA (p < 0.05) and AOPP levels (p < 0.05). There was also a significant positive correlation between all parameters. These data strongly suggest that neutrophils, which constitute the most important source of chlorinated oxidants due to their high MPO content, may be involved in serum AOPP formation and therefore the production of a novel class of pro-inflammatory mediators of oxidative stress in RA patients and that protein oxidation could play an important role in the pathogenesis of RA as does lipid peroxidation.

Serum paraoxonase 1 activity and lipid peroxidation levels in patients with age-related macular degeneration.

Our objective was to investigate antioxidant paraoxonase 1 (PON1) activity together with malondialdehyde (MDA) levels to evaluate oxidative stress in patients with age-related macular degeneration (AMD), an important cause of blindness in the elderly population. Serum PON1 activity and MDA levels were analyzed in 37 patients with AMD and compared with 29 healthy controls using a spectrophotometric method. Serum MDA levels were significantly higher in the patient group (2.76 +/- 1.28 nmol/ml) than controls (1.00 +/- 0.36 nmol/ml; p < 0.001), whereas PON1 activity was lower in the patient group (132.27 +/- 63.39 U/l) than controls (312.13 +/- 136.23 U/l; p < 0.001). There was a negative correlation between MDA and PON1 levels (r = -0.470, p < 0.001). We conclude that the observed increase in MDA levels may be related to decreased PON1 activity; the present data also demonstrated that an obvious negative correlation between PON1 activity and MDA levels exists in patients with AMD. PON1 is also an antioxidant agent, therefore effective antioxidant therapy to inhibit lipid peroxidation is necessary and agents to increase PON1 activity may be a therapeutic option in AMD.

The effect of folic acid, vitamin B6 and vitamin B12 on the homocysteine levels in rabbits fed by methionine-enriched diets.

Atherosclerosis is an important cause of cardiovascular morbidity and mortality in recent years. Hyperhomocysteinemia is recognized as an independent risk factor for premature atherosclerosis and venous thrombosis. It is suggested that administration of folic acid, vitamin B6 and vitamin B12 may decrease homocysteine levels. In our study, we induced hyperhomocysteinemia in rabbits by giving methionine and studied the effects of folic acid, vitamin B6 and vitamin B12 on homocysteine levels. A total of 40 (20 female, 20 male New Zealand rabbits) were divided into four groups, each consisting of 10 rabbits. Methionine (100 mg/kg/day), methionine (100 mg/kg/day) plus vitamin B6 (30 mg/kg/day), methionine (100 mg/kg/day) plus vitamin B12 (80 mg/kg/day) and methionine (100 mg/kg/day) plus folic acid (20 mg/kg/day) were given to the first, second, third and forth groups respectively. These rabbits were followed up for two months. We studied homocysteine levels on the 0, 20th, 40th and 60th days in all groups. In rabbits we induced hyperhomocysteinemia by giving methionine for 2 months. The decreases of homocysteine levels in the forth group were significant with respect to the second and third groups. Folic acid supplementation clearly resulted in a reduction of plasma homocysteine levels, whereas vitamin B12 was little effective and vitamin B6 failed to show an effect. We conclude that even folic acid treatment alone may be sufficient for decreasing negative effects of homocysteine.