Summer rainfall variability in European Mediterranean mountains from the sixteenth to the twentieth century reconstructed from tree rings.

Since the end of the last glacial period, European Mediterranean mountains have provided shelter for numerous species of Eurosiberian and Boreal origin. Many of these species, surviving at the southern limit of their range in Europe and surrounded by Mediterranean ones, are relatively intolerant to summer drought and are in grave danger of loss, as a result of increasingly long and frequent droughts in this region. This is the case of the Scots pine (Pinus sylvestris) and the Austrian pine (Pinus nigra ssp. salzmannii) which are found on Central Iberian Peninsula at the edge of their natural range. We used a tree ring network of these two species to reconstruct past variations in summer rainfall. The reconstruction, based upon a tree ring composite chronology of the species, dates back to 1570 (adjusted R(2) = 0.49, P < 0.000001) and captures interannual to decadal scale variability in summer precipitation. We studied the spatial representativeness of the rainfall patterns and described the occurrence rate of extremes of this precipitation. To identify associations between macroclimatic factors and tree radial growth, we employed a principal component analysis to calculate the resultant of the relationship between the growth data of both species, using this resultant as a dependent variable of a multiple regression whose independent variables are monthly mean temperature and precipitation from the average records. Spatial correlation patterns between instrumental precipitation datasets for southern Europe and reconstructed values for the 1950-1992 period indicate that the reconstruction captures the regional signal of drought variability in the study region (the origin of this precipitation is convective: thermal low pressure zones induced in the inland northeastern areas of the Iberian Peninsula). There is a clear increase in the recurrence of extreme dry events as from the beginning of twentieth century and an abrupt change to drier conditions. There appears to be a tendency toward recurrent exceptionally dry summers, which could involve a significant change for the Eurosiberian refugee species.

Is supercomplex organization of the respiratory chain required for optimal electron transfer activity?

The supra-molecular assembly of the main respiratory chain enzymatic complexes in the form of "super-complexes" has been proved by structural and functional experimental evidence. This evidence strongly contrasts the previously accepted Random Diffusion Model stating that the complexes are functionally connected by lateral diffusion of small redox molecules (i.e. Coenzyme Q and cytochrome c). This review critically examines the available evidence and provides an analysis of the functional consequences of the intermolecular association of the respiratory complexes pointing out the role of Coenzyme Q and of cytochrome c as channeled or as freely diffusing intermediates in the electron transfer activity of their partner enzymes.

[Frequency of miscarriages among pregnant women with autoimmune thyroid disorders].

AIM OF THE STUDY: To analyse the influence of antithyroid antibodies (ATA) on the frequency of spontaneous abortions (SA) by pregnant women with a normal thyroid gland function. DESIGN OF THE STUDY: Prospective clinical study on 42 selected pregnant women with a normal thyroid gland function divided into two groups: I-st group--ATA positive pregnant [n = 28] and II-end group ATA negative pregnant [n = 14]. RESULTS: Increased ATA have been found by 30 (71.4%) out of the studied 42 pregnant women. There has been no significant difference found among the values of FT3, FT4 and TSH for women with positive and negative ATA. SA have been observed at 63.3% (19/30 women) from the ATA positive ones and at 25% (4/12 women) from the ATA negative ones (P = 0.001). By the ATA positive women with SA the average values of antithyroglobulin autoantibody (Tg-Ab) (Tg-Ab positive.-189.6 +/- 49.8 IU/ml vs. Tg-Ab -negative 118.2 +/- 58.3 IU/ml, P = 0.02) and antithyroid peroxidase autoantibody (TPO-Ab) (TPO-Ab positive-176.9 +/- 57.4 IU/ml vs. TPO - negative 118.2 +/- 81.3 IU/ml, P = 0.004) are both found to be significantly higher. CONCLUSION: There is a correlation found between ATA and the increased risk of SA, where the increased concentration of ATA is combined with an increased frequency of SA.

[Is it possible to reduce the incidence of preeclampsia in pregnant women with type I diabetes mellitus].

AIM OF STUDY: To follow the meaning of diabetic metabolic control in the early pregnancy springing up the preeclampsia (PR) in pregnant women with type I diabetes mellitus (T1DM). DESIGN OF STUDY: A prospective study has been done among 105 pregnant women with T1DM. The diabetic pregnant have been divided into two groups: 1st group--43 women with preplanning pregnancy and 2nd group--62 women with non-planning pregnancy. RESULTS: There was no difference in the frequency of PR among women with planning and non-planning pregnancy (25.6% vs. 30.6%; P=0.36). The mild and moderate cases of PR among the women with planning pregnancy are prevailing, while moderate and severe cases of PR were observed in non-planning pregnancy. In pregnant women with planning pregnancy there is no difference between the initial level HbA1c of women without PR and PR (7%+/-0.7 vs. 7.1%+/-0.9%; P=0.13). Pregnant women with non-planning pregnancy have significantly higher initial level of HbA1c (9.7%+/-1.7 vs. 8.3%+/-1.3%; P=0.01). Pregnant women with PR have significantly higher body weight, creatinin, diurnal urine albumin excretion and diurnal insulin dose. CONCLUSION: The chronicle hyperglycemia in the early pregnancy in combination with the established factors are increasing the risk of preeclampsia in women with non-planning pregnancy and poor glycaemic control.

[Selenium and glutathion peroxidase enzyme levels in diabetic patients with early spontaneous abortions].

UNLABELLED: The incidence of spontaneous abortions in women with type 1 diabetes mellitus varies between 10-30%. The etiology of this is still unclear despite numerous experimental studies. Pregnancy is a condition of increased oxidative stress due to impaired balance between pro- and antioxidants. Glutathion and related enzymes perform the best antioxidant protection. Some authors point to a possible correlation between spontaneous abortions and low plasma Se levels as well as low intracellular activity of glutathion peroxidase enzyme. Others report that Hb A1-c, values over 1SD above normal increase the risk of spontaneous abortions with 3% and Hb A1-C values between 10-12% are critically high for the occurrence of spontaneous abortions. The purpose of the study was to evaluate the levels of Se and glutathion peroxidase enzyme (Gl-Px) in pregnant women with type 1 diabetes mellitus in the first trimester of pregnancy and to find out is there a correlation between glycemic control of diabetes and the incidence of spontaneous abortions. DESCRIPTION OF PROJECT: 75 pregnant women enrolled in an- 1 year prospective study divided in 3 groups according to pregnancy outcome: gr. 1 - n = 30 with type diabetes mellitus, no abortions, gr.2 - n = 16 with type diabetes mellitus with first trimester spontaneous abortion and gr. 3 - n = 29 healthy pregnant women. Women with type 1 diabetes mellitus were divided into three subgr. according to glycemic control - subgr. 1 - n = 12 (Hb A1-c < 7%), subgr.2 - n = 18 (Hb A1-c > 7< 8%), subgr.3 - n = 16 (Hb A1-c > 8%). Gl-Px activity was determined in Er hemolisate with test reagents of Randox Ransel, with ref.values 27.5 - 73 U/g Hb. Selen concentration was determined in whole blood sample by atomic absorption spectrophotometry with ref. values 0.12-1.1 micromol/l. HbA 1-C was measured by affinity chromatography with ref. values 4.5-6.3%. Statistical methods used were: dispersion, correlation analysis - SPSS package version 11.01.01. RESULTS: Basic Se levels were low in all pregnant women in early pregnancy. The metabolic control level did not influence the levels of Se in pregnant women with diabetes mellitus type1. Gl -Px activity was within the normal limits in all women. There was no correlation between Se levels and Gl -Px activity in pregnant diabetics with and without abortions. There was a correlation between Se levels and Gl -Px activity only in healthy pregnant women. Pregnant women with poor glycemic control had higher incidence of spontaneous abortions. CONCLUSIONS: We could not support the hypothesis of reduced antioxidant protection (low Se and Gl-Px levels) as a causative factor in the pathogenesis of spontaneous abortions in diabetic patients. Our study results showed that poor metabolic control of diabetes (high Hb A1-c) in the first trimester of pregnancy had a primary role in the occurrence of early abortions. We could speculate that the early hyperglycemic maternal-fetal environment most probably plays a role of an additional stress to the developing embryo.

Mitochondrial bioenergetics in aging.

Mitochondria are strongly involved in the production of reactive oxygen species, considered as the pathogenic agent of many diseases and of aging. The mitochondrial theory of aging considers somatic mutations of mitochondrial DNA induced by oxygen radicals as the primary cause of energy decline; experimentally, complex I appears to be mostly affected and to become strongly rate limiting for electron transfer. Mitochondrial bioenergetics is also deranged in human platelets upon aging, as shown by the decreased Pasteur effect (enhancement of lactate production by respiratory chain inhibition). Cells counteract oxidative stress by antioxidants; among lipophilic antioxidants, coenzyme Q is the only one of endogenous biosynthesis. Exogenous coenzyme Q, however, protects cells from oxidative stress by conversion into its reduced antioxidant form by cellular reductases.

[Glucooxidative stress and spontaneous abortion in pregnant women with diabetes mellitus type 1].

UNLABELLED: The pregnancies in women with Diabetes mellitus are in condition of increased glucooxidative stress, which could be toxic for the developing embryo. END-POINTS: To evaluate the levels of selenium and glutation peroxidase in pregnant women with Diabetes mellitus type 1 in the first trimester of pregnancy and to establish whether there is a correlation between the diabetic glycemic control and occurrence of spontaneous abortions. STUDY DESIGN: Prospective study of 75 women for 1 year period. he pregnant women were divided in 3 groups as follows: 1st group--30 pregnant women with Diabetes mellitus type 1 with normal outcome; 2nd group--16 pregnant women with Diabetes mellitus type 1 with spontaneous abortion; 3rd group--29 healthy pregnant controls. The activity of GI-Px in red blood cells was measured in hemolysat of EDTA plasma in Germany. The levels of glucosylated haemoglobin were also evaluated. RESULTS: 1. In all pregnant women the levels of selenium were lower without significant difference between them 1st group--0.12 +/- 0.6 mmol/l, 2ndd group 0.13 +/- 0.1 mmol/l, 3rd group 0.13 +/- 0.7 mmol/l (P > 0.05). 2. There is an increase in the activity of GI-Px, which is statistically significant in the healthy pregnant women 47.8 +/- 13.3 U/g Hb and diabetic pregnant women with normal outcome 48. 6 +/- 8.4 U/g Hb. There is no statistically significant difference in the activity of GI-Px in diabetic pregnant women with spontaneous abortions and the healthy controls (P > 0. 05). 3. Negative correlation between the levels of selenium and the activity of GI-Px was proved in healthy pregnant women (r = - 0.4; P < 0.05). No correlation was found between the level of the selenium and the activity of GI-Px into the two groups of diabetic pregnant women. 4. There is a correlation in the levels of diabetic pregnant women with spontaneous abortions (r = -0.38; P < 0.001). CONCLUSIONS: The increased activity of GI-Px in diabetic pregnant women with spontaneous abortions is a result of increased antioxidative defense of the cell. Probably the ineffective antioxidant defense, leading to a spontaneous abortion is due to the low levels of selenium and high level of pre-prandial glycaemia.

[The frequency of mild and severe fetal malformations in diabetic women with high values of glycosilated hemoglobin in early pregnancy].

PURPOSE: To evaluate the correlation between maternal hyperglycemia in early pregnancy and the risk of fetal abnormalities in pregnant women with type 1 diabetes mellitus. STUDY DESIGN: A retrospective study over 124 pregnant women with diabetes mellitus type 1 hospitalized in High Risk Pregnancy Department--SHATOG "Maichin dom" has been done from January. 1998 to January 2004. The diabetic pregnant women were divided in two groups: first group pregnant women without malformations n = 105 and second group pregnant women with malformations n = 19. The pregnant women with fetal malformations were divided into two subgroups: with major malformations n = 13 and with minor malformations n = 6. The diabetic pregnant women were divided in classes according to Whites Classification: Class B - 38, Class C - 35; Class D - 39 and Class R/F - 12. The values of preprandial glucose, postprandial glucose and glycosilated hemoglobin has been measured at 13 week of gestation. RESULTS: 104 pregnancies of total 124 pregnancies were without abnormalities. The fetal malformations were observed in 19 (15.3%) of total 124 pregnancies. The rate of major abnormalities were - 13 (10.4%) and minor abnormalities were - 7 (5.6%). The highest rate of abnormalities there has been within the complicated diabetic women of class D - n = 7 (17.9 %) and class R/F n = 3 (25%). The initial values of preprandial glucose 9.54 (SD +/- 3.59) mmol/l and postprandiai glucose 10.52 (SD +/- 1.81) mmol/l between the women whit pregnancies with abnormalities were significantly higher then those values of preprandial glucose 7.39 (SD +/- 2.82) mmol/l (P - 0.021) and values of postprandial glucose 10.52 (SD +/- 1.81) mmol/l (P = 0.014) between the women without fetal malformations. The mean values of glycosilated hemoglobin were significantly higher HbA 1 c = 9. 01% (SD +/- 1.53) in pregnancies complicated with malformations than those values measured in pregnancies without fetal malformations 8.06% (SD +/- 1.64, P = 0.022). A positive correlation between the observed abnormalities and metabolic control in the early pregnancy exist. The values of Hbeta A1-c is significantly higher Hbeta A1-c - 9.9% (SD +/- 1.2) in pregnancies complicated with fetal malformations than those measured in pregnancies without malformations. Hbeta A1-c 8.2% (SD +/- 1.5) n = 125. Significant differences in the value of Hbeta A1-c between pregnancies with mild and those with severe abnormalities have not been established. A correlation between the levels of Hbeta A1-c in early pregnancy and the rate of the observed abnormalities exist. Within the values of Hbeta A1-c < 7.9%, the rate of malformations is 6.9%, Hbeta A1-c > 8.0% < 10%, the rate of malformations is 19.0% and within the values of Hbeta A1-c > 10%, the rate of the observed abnormalities is 31.5%. A logistic regression between the higher values of postprandial glucose and Hbeta A1-c values and the relative risk of congenital malformations has been observed. The relative risk is evaluated by odds ratio (OR) When the levels of Hbeta A1-c rise with 1% the relative risk of congenital malformations is evaluated by odds ratio OR = 2.02 (limited in 1.46 - 2.81 by 95% conf. interval) and when the levels of postprandial glucose rise with 1 mmol/l the relative risk OR = 1.21 (limited in 1.06 - 1.37: 95% conf. interval). CONCLUSION: Fetal abnormalities are more frequent in pregnant women with long lasting diabetes complicated with vasculopathy. Fetal abnormalities are associated with higher levels of Hbeta A1-c in the first trimester of pregnancy. In diabetic women who planed their pregnancy an optimal metabolic control must been established.

Uptake and distribution of exogenous CoQ in the mitochondrial fraction of perfused rat liver.

The system of perfusing rat livers has been used to evaluate the uptake and incorporation of liposomal CoQ10 into mitochondria. After 90 minutes of perfusion the cells are strongly enriched in CoQ10 up to levels of the same order of magnitude as CoQ9. Heavy and light mitochondrial crude subcellular fractions, low in CoQ10 in control livers, contain high amounts of the quinone after perfusion; yet the purification of these fractions on a metrizamide gradient reveals that the exogenous quinone is mainly associated with the light mitochondrial subfraction, enriched in lysosomes. An increase of the NAD-dependent glutamate-malate oxidase activity is observed in CoQ10 perfused animals. As the total levels of CoQ9 + CoQ10 in these animals are not significantly modified by the CoQ10 incorporated, the observed higher activity is not ascribable to an integration of exogenous quinone into the ubiquinone pool. An antioxidant effect of extramitochondrial CoQ10 on mitochondrial functions is suggested.

Coenzyme Q changes in liver and plasma in the rat after partial hepatectomy.

The levels of coenzyme Q were determined in blood plasma and regenerating liver mitochondria of hepatectomized rats, using as controls either sham-operated or non-operated animals. Mitochondrial CoQ9 content increased in sham-operated rats, whereas it was significantly lower in hepatectomized with respect to non-operated animals. Plasma CoQ9 levels decreased dramatically in hepatectomized animals, but increased strongly in sham-operated in comparison with non-operated rats. The data suggest the possibility of a rate-limiting step in CoQ biosynthesis in hepatectomized animals.

Underevaluation of complex I activity by the direct assay of NADH-coenzyme Q reductase in rat liver mitochondria.

We have shown that the rate of NADH-coenzyme Q reductase in rat liver mitochondria, assayed using the decyl-ubiquinone analog DB, is underevaluated, probably as a result of its low water solubility. In view of drawbacks encountered using other more soluble acceptors in this system, we demonstrate that the most reliable assay of the physiological rate of CoQ reduction by Complex I is the indirect calculation from the total rate of NADH oxidation and the rate of ubiquinol oxidation, using the pool equation of Kröger and Klingenberg [(1973) Eur. J. Biochem. 34, 358-368].

The site of production of superoxide radical in mitochondrial Complex I is not a bound ubisemiquinone but presumably iron-sulfur cluster N2.

The mitochondrial respiratory chain is a powerful source of reactive oxygen species, considered as the pathogenic agent of many diseases and of aging. We have investigated the role of Complex I in superoxide radical production in bovine heart submitochondrial particles and found, by combined use of specific inhibitors of Complex I and by Coenzyme Q (CoQ) extraction from the particles, that the one-electron donor in the Complex to oxygen is a redox center located prior to the binding sites of three different types of CoQ antagonists, to be identified with a Fe-S cluster, most probably N2 on the basis of several known properties of this cluster. Short chain CoQ analogs enhance superoxide formation, presumably by mediating electron transfer from N2 to oxygen. The clinically used CoQ analog, idebenone, is particularly effective in promoting superoxide formation.

Decrease of rotenone inhibition is a sensitive parameter of complex I damage in brain non-synaptic mitochondria of aged rats.

We investigated NADH oxidation in non-synaptic and synaptic mitochondria from brain cortex of 4- and 24-month-old rats. The NADH oxidase activity was significantly lower in non-synaptic mitochondria from aged rats; we also found a significant decrease of sensitivity of NADH oxidation to the specific Complex I inhibitor, rotenone. Since the rotenone-binding site encompasses Complex I subunits encoded by mtDNA, these results are in accordance with the mitochondrial theory of aging, whereby somatic mtDNA mutations are at the basis of cellular senescence. Accordingly, a 5 kb deletion was detected only in the cortex of the aged animals.

Inhibitor sensitivity of respiratory complex I in human platelets: a possible biomarker of ageing.

NADH-Coenzyme Q reductase was assayed in platelet mitochondrial membranes obtained from 19 pools of two venous blood samples from female young (19-30 years) individuals and 18 pools from aged ones (66-107 years). The enzyme activities were not significantly changed in the two groups, but a decrease of sensitivity to the specific inhibitor, rotenone, occurred in a substantial number of aged individuals. The results are in agreement with the predictions of the mitochondrial theory of ageing and may be used to develop a sensitive biomarker of the ageing process.

Coenzyme Q content in synaptic and non-synaptic mitochondria from different brain regions in the ageing rat.

We investigated the Coenzyme Q (CoQ) content of different mitochondrial fractions [free mitochondria (FM), synaptic heavy (HM) and light mitochondria (LM)] from three brain areas (cortex, striatum, hippocampus) of rats at different ages. In rats from 2 to 26 months of age, we observed only small differences in total CoQ content (CoQ9 + CoQ10). In FM and LM fractions, values are very similar and appear to be much higher than in HM fractions. The CoQ10/CoQ9 ratios are much higher in brain mitochondria than in other organs, suggesting possible modifications of CoQ biosynthetic pathways in brain; nevertheless they appear to remain constant during ageing. CoQ9 and CoQ10 contents slowly decrease reaching their minimum in rats of 18 months of age, then increase in the older ages. Considering ageing as partially driven by a summation of free radical-mediated processes, we can hypothesize that damage occurring to biological structures in the first half of life might be followed by induction phenomena tending to re-establish the primitive levels of antioxidant molecules.

Cytotoxic efficacy of bendamustine in human leukemia and breast cancer cell lines.

PURPOSE: The purpose of this study was to characterise bendamustine's cytotoxic and apoptotic activity in a panel of leukemia and breast cancer cell lines in comparison to its clastogenicity in murine bone marrow. METHODS: The cytotoxic effect of bendamustine was measured by the 3-(4,5-dimethylthiazol-2-yl)-2,5 diphenyltetrazolium bromide (MTT)-dye reduction assay. Induction of apoptosis was evidenced by DNA gel electrophoresis, nuclear staining, Western blot poly-(adenosine diphosphate-ribose) polymerase (PARP) cleavage, and flow cytometry. As a measure of hematological toxicity, the formation of chromosomal aberrations was investigated in bone marrow cells isolated from mice treated with low non-toxic doses of bendamustine and lomustine. RESULTS: Bendamustine was preferably active against leukemic cells of lymphoid origin and was found to induce apoptosis in SKW-3 and BV-173 cells as shown by oligonucleosomal DNA and nuclear fragmentation, PARP cleavage, and formation of a sub-G1 fraction. Myeloid and breast carcinoma cell lines were resistant towards bendamustine with the exception of HL-60 cells which exhibit an intermediate sensitivity. Bendamustine was found to have a very low clastogenic effect as compared with equimolar doses of lomustine. CONCLUSION: Taken together, the mode of action of bendamustine includes induction of apoptosis. The specific spectrum of activity and the unexpectedly low clastogenicity support the hypothesis that bendamustine in not a typical alkylating agent but exerts an additional mode of action, possibly as a purine antimetabolite.

Mitochondrial respiratory chain features after gamma-irradiation.

Radiation provokes damage to DNA but also to membrane and protein structure. Radiolysis is a tool used very often in the study of free radical biological effects and of scavenger molecules effectiveness. Nitroimidazoles have been demonstrated to enhance the radiation effects on biological structures. The studies we have performed on isolated mitochondria irradiated, with and without nitroimidazoles, at a radiation dose equal to LD90, indicate that this treatment is not able to affect the structural and functional features investigated (ubiquinone-10, fatty acids, respiratory cytochrome levels or membrane fluidity and respiratory enzymatic activities), suggesting that an involvement of such externally produced radicals on membrane damage is unlikely. Moreover it was ascertained that the mitochondrial redox activities do not take part into the intracellular nitroimidazole reduction.

Serum cystatin C in renal transplant patients.

Assessment of renal function in clinical medicine is of great importance especially in patients with renal transplants. Cystatin C has the characteristics of an ideal marker to assess renal glomerular filtration rate. Forty patients with renal transplants under steady-state post-transplant conditions were included in the study. Steady-state was defined as lack of acute rejection periods during the last 6 months and stable cyclosporin A medication during the past 4 weeks. Gender was balanced with 20 male and 20 female patients, the mean age was 51+/-14 years, time since transplantation was 5+/-3.5 years. Fifteen percent of the patients suffered from diabetes mellitus. Immunosuppression consisted of cyclosporin A, imuran, and prednisolon. To assess renal function cystatin C, creatinine clearance, serum creatinine, and serum beta2-microglobulin were tested. Creatinine was analysed in serum and urine to calculate the creatinine clearance related to 1.73 m(2) body surface. Cystatin C and beta2-microglobulin were determined by using a particle-enhanced turbidimetric assay. Cystatin C correlated best with creatinine clearance (r=0.66), beta2-microglobulin (0.57), and serum creatinine (0.56). The diagnostic accuracy of cystatin C was significantly better than serum creatinine (p<0.05), but did not differ significantly from creatinine clearance (p=0.73), and beta2-microglobulin (p=0.46). Our data show that patients with renal transplants, cystatin C has a similar diagnostic value as creatinine clearance. However, it is superior to serum determination of creatinine and beta2-microglobulin. Cystatin C allows for rapid and accurate assessment of renal function in patients with renal transplants and is clearly superior to the commonly used serum creatinine.

Localization and mobility of coenzyme Q in lipid bilayers and membranes.

We have studied the mobility of coenzyme Q (CoQ) in lipid bilayers and mitochondrial membranes in relation to the control of electron transfer activities. A molecular dynamics computer simulation in the vacuum yielded a folded structure for CoQ10, with a length of only 21 A. Using this information we were able to calculate diffusion coefficients in the range of 10(-6) cm2/s in good agreement with those found experimentally by fluorescence quenching of pyrene derivatives. To investigate if CoQ diffusion may represent the rate-limiting step of electron transfer, we reconstituted complexes I and III and assayed the resulting NADH-cytochrome c reductase activity in presence of different CoQ10 levels and at different distances between complexes; the experimental turnovers were higher than the collision frequencies calculated using diffusion coefficients of 10(-9) cm2/s but compatible with values found by us by fluorescence quenching. Since the experimental turnovers are independent of the distance between complexes, we conclude that CoQ diffusion is not rate-limiting for electron transfer.

Protective effect of exogenous coenzyme Q in rats subjected to partial hepatic ischemia and reperfusion.

In a surgical model of liver ischemia lipid peroxidation occurs, as shown by increase of lipid peroxidation end products, endogenous CoQ9 is oxidized and mitochondrial respiration is lowered; however, pre-treatment of the rats by i.p. injection of CoQ10 for 14 days normalizes the above parameters, presumably by way of the observed high extent of reduction of the incorporated quinone; moreover, liver homogenates of the CoQ10-treated rats are more resistant than those of non-treated rats to oxidative stress induced by an azido free radical initiator. This preliminary study suggests that CoQ10 pre-treatment can be of beneficial effect against oxidative damage during liver surgery transplantation.