Sándor Pintér - Academia.edu (original) (raw)
Papers by Sándor Pintér
Blood Cells Molecules and Diseases, 2000
The glutathione redox system and alpha-tocopherol, both of which are essential for maintaining th... more The glutathione redox system and alpha-tocopherol, both of which are essential for maintaining the normal structure of biological membranes, some other lipid-soluble antioxidants (lycopene, beta-carotene, retinol), and lipid peroxidation, were investigated in the blood from two triosephosphate isomerase (TPI)-deficient brothers. Both of the genetically identical compound heterozygote brothers have congenital hemolytic anemia, but only one of them has a neurological defect, the second cardinal symptom of TPI deficiency. Whole blood reduced glutathione levels were markedly decreased in both brothers. The glutathione reductase activities as well as the NADPH contents of their erythrocytes were in the normal range or slightly enhanced. Increased ratio of oxidized/reduced glutathione, elevated glutathione S-transferase activity, and increased d-lactate level, a metabolite of the glyoxalase pathway, were detected only in the neurologically affected propositus. The plasma carotenoids (lycopene + beta-carotene), alpha-tocopherol/cholesterol + triglyceride ratios, and the erythrocyte alpha-tocopherol levels were significantly decreased in both patients. It seems conceivable that membrane alterations due to the low level of these reducing agents may contribute to the shortened life span of erythrocytes. The imbalance of the prooxidant/antioxidant homeostasis as well as the increased rate of methylglyoxal formation may also have been involved in the development of the neurological manifestations in the propositus.
European Journal of Obstetrics & Gynecology and Reproductive Biology, 2001
Objective: Our objective was to determine whether two methylxanthines, pentoxifylline (PTX) and a... more Objective: Our objective was to determine whether two methylxanthines, pentoxifylline (PTX) and allopurinol, would have bene®cial effects on experimental pregnancy-induced pre-eclampsia-like disease in ewes.
Biochemical and Molecular Medicine, 1997
the primary cause of pregnancy-induced hyperten-Toxicosis syndrome of fasting pregnant ewes has s... more the primary cause of pregnancy-induced hyperten-Toxicosis syndrome of fasting pregnant ewes has sion. ᭧ 1997 Academic Press a close similarity to human preeclampsia (hypertension, albuminuria). The common etiological fac-Pregnancy-induced hypertension (PIH), usually tor might be oxidative hemolysis and heme-inmanifested in late gestation, is a major cause of fetal duced endothelial damage. Ewes (5 starving, 5 conand maternal morbidity and mortality. If associated trol) at 130 -135 gestational days with a 96-h fasting with albuminuria, edema, or both, the disease is period followed by refeeding were used. Blood termed preeclampsia (1). A severe and acute complipressure, platelet count, electrolytes, kidney and liver function parameters, as well as plasma glu-cation of preeclampsia is the Hemolysis, Elevated cose, hemoglobin/heme, free thiol groups and Tro-Liver enzymes, and Low Platelet count syndrome lox equivalent antioxidant capacity, and plasma (HELLP syndrome) (2).
Journal of Clinical Virology, 2005
Journal of Clinical Virology, 2006
Blood Cells Molecules and Diseases, 2000
The glutathione redox system and alpha-tocopherol, both of which are essential for maintaining th... more The glutathione redox system and alpha-tocopherol, both of which are essential for maintaining the normal structure of biological membranes, some other lipid-soluble antioxidants (lycopene, beta-carotene, retinol), and lipid peroxidation, were investigated in the blood from two triosephosphate isomerase (TPI)-deficient brothers. Both of the genetically identical compound heterozygote brothers have congenital hemolytic anemia, but only one of them has a neurological defect, the second cardinal symptom of TPI deficiency. Whole blood reduced glutathione levels were markedly decreased in both brothers. The glutathione reductase activities as well as the NADPH contents of their erythrocytes were in the normal range or slightly enhanced. Increased ratio of oxidized/reduced glutathione, elevated glutathione S-transferase activity, and increased d-lactate level, a metabolite of the glyoxalase pathway, were detected only in the neurologically affected propositus. The plasma carotenoids (lycopene + beta-carotene), alpha-tocopherol/cholesterol + triglyceride ratios, and the erythrocyte alpha-tocopherol levels were significantly decreased in both patients. It seems conceivable that membrane alterations due to the low level of these reducing agents may contribute to the shortened life span of erythrocytes. The imbalance of the prooxidant/antioxidant homeostasis as well as the increased rate of methylglyoxal formation may also have been involved in the development of the neurological manifestations in the propositus.
European Journal of Obstetrics & Gynecology and Reproductive Biology, 2001
Objective: Our objective was to determine whether two methylxanthines, pentoxifylline (PTX) and a... more Objective: Our objective was to determine whether two methylxanthines, pentoxifylline (PTX) and allopurinol, would have bene®cial effects on experimental pregnancy-induced pre-eclampsia-like disease in ewes.
Biochemical and Molecular Medicine, 1997
the primary cause of pregnancy-induced hyperten-Toxicosis syndrome of fasting pregnant ewes has s... more the primary cause of pregnancy-induced hyperten-Toxicosis syndrome of fasting pregnant ewes has sion. ᭧ 1997 Academic Press a close similarity to human preeclampsia (hypertension, albuminuria). The common etiological fac-Pregnancy-induced hypertension (PIH), usually tor might be oxidative hemolysis and heme-inmanifested in late gestation, is a major cause of fetal duced endothelial damage. Ewes (5 starving, 5 conand maternal morbidity and mortality. If associated trol) at 130 -135 gestational days with a 96-h fasting with albuminuria, edema, or both, the disease is period followed by refeeding were used. Blood termed preeclampsia (1). A severe and acute complipressure, platelet count, electrolytes, kidney and liver function parameters, as well as plasma glu-cation of preeclampsia is the Hemolysis, Elevated cose, hemoglobin/heme, free thiol groups and Tro-Liver enzymes, and Low Platelet count syndrome lox equivalent antioxidant capacity, and plasma (HELLP syndrome) (2).
Journal of Clinical Virology, 2005
Journal of Clinical Virology, 2006
Journal of Histochemistry & Cytochemistry, 2008
S U M M A R Y The functional recovery of skeletal muscles after peripheral nerve transection and ... more S U M M A R Y The functional recovery of skeletal muscles after peripheral nerve transection and microsurgical repair is generally incomplete. Several reinnervation abnormalities have been described even after nerve reconstruction surgery. Less is known, however, about the regenerative capacity of reinnervated muscles. Previously, we detected remarkable morphological and motor endplate alterations after inducing muscle necrosis and subsequent regeneration in the reinnervated rat soleus muscle. In the present study, we comparatively analyzed the morphometric properties of different fiber populations, as well as the expression pattern of myosin heavy chain isoforms at both immunohistochemical and mRNA levels in reinnervated versus reinnervated-regenerated muscles. A dramatic slow-tofast fiber type transition was found in reinnervated soleus, and a further change toward the fast phenotype was observed in reinnervated-regenerated muscles. These findings suggest that the (fast) pattern of reinnervation plays a dominant role in the specification of fiber phenotype during regeneration, which can contribute to the long-lasting functional impairment of the reinnervated muscle. Moreover, because the fast II fibers (and selectively, a certain population of the fast IIB fibers) showed better recovery than did the slow type I fibers, the faster phenotype of the reinnervated-regenerated muscle seems to be actively maintained by selective yet undefined cues. (J Histochem Cytochem 56:111-123, 2008)
The regeneration of skeletal muscles is a suitable model to study the development and differentia... more The regeneration of skeletal muscles is a suitable model to study the development and differentiation of contractile tissues. Neural effects are one of the key factors in the regulation of this process. In the present work, effects of different reinnervation protocols (suture or grafting) were studied upon the regenerative capacity of rat soleus muscles treated with the venom of the Australian tiger snake, notexin, which is known to induce complete necrosis and subsequent regeneration of muscles. Morphological and motor endplate analysis indicated that the regenerative capacity of denervated, and thereafter surgically reinnervated muscles remains impaired compared to that of normally innervated muscles, showing differences in the muscle size, fiber type pattern and motor endplate structure, even 35 days after the notexin injection. A lack or deficiency of secreted neural factors, deterioration of satellite cells and/or incomplete recovery of the sutured or grafted nerves may be the cause of these discrepancies in the regeneration process.
Neuromuscular Disorders, 2006
Disuse induces skeletal muscle atrophy, but the molecular mechanism is largely unknown. In partic... more Disuse induces skeletal muscle atrophy, but the molecular mechanism is largely unknown. In particular, involvement of dystrophin glycoprotein complex (DGC), the main component of the sarcolemma, in disuse-induced muscle atrophy has not been fully examined. Twelve-week-old female C57BL/6 mice and neuronal nitric oxide synthase (nNOS)-null mice were randomly assigned to control or tail-suspension group. To induce muscle atrophy, the tail of the mouse was suspended from the top of the cage for 14 days. Skeletal muscles of the hind limbs were examined. We found that nNOS, a multifunctional regulator that is located at the sarcolemma as a member of DGC, quickly disappeared from the sarcolemma and was dislocated to the cytoplasm during tail suspension. Tail suspension-induced muscle atrophy was considerably relieved in nNOS-null mice. Furthermore, a nNOS-specific inhibitor significantly prevented suspension-induced muscle atrophy. nNOS can be a key molecule of molecular pathology of disuse-induced muscle atrophy. We, therefore, measured nitric oxide (NO) in skeletal muscle of living mice by using electron paramagnetic spectrometry and found that NO production was elevated in atrophied muscle, suggesting that NO is a possible mediator of muscle atrophy. Up-regulation of muscle atrophy-related E3 ubiquitin-ligases (MuRF-1 and Atrogin-1) and nuclear accumulation of de-phosphorylated Foxo3a were not evident in nNOS-null muscle after tail suspension. On the other hand, neither NFjB nor the Akt/S6k1/mTOR pathway is under the control of NO. The number of apoptotic myonuclei in tail-suspended nNOS-null mice was less than 20 % of that of tail-suspended wild-type mice. Glyceraldehyde-3-phosphate dehydrogenase (GAP-DH) was found to be nitrosated and removed to the nucleus in atrophied muscle together with an E3 ubiquitin-ligase, Siah-1. These findings strongly suggest that nitrosation of GAPDH by NO triggers apoptotic changes in myonuclei. In muscle biopsy specimens of neurogenic muscle atrophy such as amyotrophic lateral sclerosis, dislocation of nNOS was also observed in immunohistochemical study. We can conclude that dislocation of nNOS to the cytoplasm and overproduction of NO result in suspension-induced muscle atrophy. Pharmacological treatment to antagonize nNOS/NO can be a new therapeutic strategy to prevent muscle atrophy.
Blood Cells Molecules and Diseases, 2000
The glutathione redox system and alpha-tocopherol, both of which are essential for maintaining th... more The glutathione redox system and alpha-tocopherol, both of which are essential for maintaining the normal structure of biological membranes, some other lipid-soluble antioxidants (lycopene, beta-carotene, retinol), and lipid peroxidation, were investigated in the blood from two triosephosphate isomerase (TPI)-deficient brothers. Both of the genetically identical compound heterozygote brothers have congenital hemolytic anemia, but only one of them has a neurological defect, the second cardinal symptom of TPI deficiency. Whole blood reduced glutathione levels were markedly decreased in both brothers. The glutathione reductase activities as well as the NADPH contents of their erythrocytes were in the normal range or slightly enhanced. Increased ratio of oxidized/reduced glutathione, elevated glutathione S-transferase activity, and increased d-lactate level, a metabolite of the glyoxalase pathway, were detected only in the neurologically affected propositus. The plasma carotenoids (lycopene + beta-carotene), alpha-tocopherol/cholesterol + triglyceride ratios, and the erythrocyte alpha-tocopherol levels were significantly decreased in both patients. It seems conceivable that membrane alterations due to the low level of these reducing agents may contribute to the shortened life span of erythrocytes. The imbalance of the prooxidant/antioxidant homeostasis as well as the increased rate of methylglyoxal formation may also have been involved in the development of the neurological manifestations in the propositus.
European Journal of Obstetrics & Gynecology and Reproductive Biology, 2001
Objective: Our objective was to determine whether two methylxanthines, pentoxifylline (PTX) and a... more Objective: Our objective was to determine whether two methylxanthines, pentoxifylline (PTX) and allopurinol, would have bene®cial effects on experimental pregnancy-induced pre-eclampsia-like disease in ewes.
Biochemical and Molecular Medicine, 1997
the primary cause of pregnancy-induced hyperten-Toxicosis syndrome of fasting pregnant ewes has s... more the primary cause of pregnancy-induced hyperten-Toxicosis syndrome of fasting pregnant ewes has sion. ᭧ 1997 Academic Press a close similarity to human preeclampsia (hypertension, albuminuria). The common etiological fac-Pregnancy-induced hypertension (PIH), usually tor might be oxidative hemolysis and heme-inmanifested in late gestation, is a major cause of fetal duced endothelial damage. Ewes (5 starving, 5 conand maternal morbidity and mortality. If associated trol) at 130 -135 gestational days with a 96-h fasting with albuminuria, edema, or both, the disease is period followed by refeeding were used. Blood termed preeclampsia (1). A severe and acute complipressure, platelet count, electrolytes, kidney and liver function parameters, as well as plasma glu-cation of preeclampsia is the Hemolysis, Elevated cose, hemoglobin/heme, free thiol groups and Tro-Liver enzymes, and Low Platelet count syndrome lox equivalent antioxidant capacity, and plasma (HELLP syndrome) (2).
Journal of Clinical Virology, 2005
Journal of Clinical Virology, 2006
Blood Cells Molecules and Diseases, 2000
The glutathione redox system and alpha-tocopherol, both of which are essential for maintaining th... more The glutathione redox system and alpha-tocopherol, both of which are essential for maintaining the normal structure of biological membranes, some other lipid-soluble antioxidants (lycopene, beta-carotene, retinol), and lipid peroxidation, were investigated in the blood from two triosephosphate isomerase (TPI)-deficient brothers. Both of the genetically identical compound heterozygote brothers have congenital hemolytic anemia, but only one of them has a neurological defect, the second cardinal symptom of TPI deficiency. Whole blood reduced glutathione levels were markedly decreased in both brothers. The glutathione reductase activities as well as the NADPH contents of their erythrocytes were in the normal range or slightly enhanced. Increased ratio of oxidized/reduced glutathione, elevated glutathione S-transferase activity, and increased d-lactate level, a metabolite of the glyoxalase pathway, were detected only in the neurologically affected propositus. The plasma carotenoids (lycopene + beta-carotene), alpha-tocopherol/cholesterol + triglyceride ratios, and the erythrocyte alpha-tocopherol levels were significantly decreased in both patients. It seems conceivable that membrane alterations due to the low level of these reducing agents may contribute to the shortened life span of erythrocytes. The imbalance of the prooxidant/antioxidant homeostasis as well as the increased rate of methylglyoxal formation may also have been involved in the development of the neurological manifestations in the propositus.
European Journal of Obstetrics & Gynecology and Reproductive Biology, 2001
Objective: Our objective was to determine whether two methylxanthines, pentoxifylline (PTX) and a... more Objective: Our objective was to determine whether two methylxanthines, pentoxifylline (PTX) and allopurinol, would have bene®cial effects on experimental pregnancy-induced pre-eclampsia-like disease in ewes.
Biochemical and Molecular Medicine, 1997
the primary cause of pregnancy-induced hyperten-Toxicosis syndrome of fasting pregnant ewes has s... more the primary cause of pregnancy-induced hyperten-Toxicosis syndrome of fasting pregnant ewes has sion. ᭧ 1997 Academic Press a close similarity to human preeclampsia (hypertension, albuminuria). The common etiological fac-Pregnancy-induced hypertension (PIH), usually tor might be oxidative hemolysis and heme-inmanifested in late gestation, is a major cause of fetal duced endothelial damage. Ewes (5 starving, 5 conand maternal morbidity and mortality. If associated trol) at 130 -135 gestational days with a 96-h fasting with albuminuria, edema, or both, the disease is period followed by refeeding were used. Blood termed preeclampsia (1). A severe and acute complipressure, platelet count, electrolytes, kidney and liver function parameters, as well as plasma glu-cation of preeclampsia is the Hemolysis, Elevated cose, hemoglobin/heme, free thiol groups and Tro-Liver enzymes, and Low Platelet count syndrome lox equivalent antioxidant capacity, and plasma (HELLP syndrome) (2).
Journal of Clinical Virology, 2005
Journal of Clinical Virology, 2006
Journal of Histochemistry & Cytochemistry, 2008
S U M M A R Y The functional recovery of skeletal muscles after peripheral nerve transection and ... more S U M M A R Y The functional recovery of skeletal muscles after peripheral nerve transection and microsurgical repair is generally incomplete. Several reinnervation abnormalities have been described even after nerve reconstruction surgery. Less is known, however, about the regenerative capacity of reinnervated muscles. Previously, we detected remarkable morphological and motor endplate alterations after inducing muscle necrosis and subsequent regeneration in the reinnervated rat soleus muscle. In the present study, we comparatively analyzed the morphometric properties of different fiber populations, as well as the expression pattern of myosin heavy chain isoforms at both immunohistochemical and mRNA levels in reinnervated versus reinnervated-regenerated muscles. A dramatic slow-tofast fiber type transition was found in reinnervated soleus, and a further change toward the fast phenotype was observed in reinnervated-regenerated muscles. These findings suggest that the (fast) pattern of reinnervation plays a dominant role in the specification of fiber phenotype during regeneration, which can contribute to the long-lasting functional impairment of the reinnervated muscle. Moreover, because the fast II fibers (and selectively, a certain population of the fast IIB fibers) showed better recovery than did the slow type I fibers, the faster phenotype of the reinnervated-regenerated muscle seems to be actively maintained by selective yet undefined cues. (J Histochem Cytochem 56:111-123, 2008)
The regeneration of skeletal muscles is a suitable model to study the development and differentia... more The regeneration of skeletal muscles is a suitable model to study the development and differentiation of contractile tissues. Neural effects are one of the key factors in the regulation of this process. In the present work, effects of different reinnervation protocols (suture or grafting) were studied upon the regenerative capacity of rat soleus muscles treated with the venom of the Australian tiger snake, notexin, which is known to induce complete necrosis and subsequent regeneration of muscles. Morphological and motor endplate analysis indicated that the regenerative capacity of denervated, and thereafter surgically reinnervated muscles remains impaired compared to that of normally innervated muscles, showing differences in the muscle size, fiber type pattern and motor endplate structure, even 35 days after the notexin injection. A lack or deficiency of secreted neural factors, deterioration of satellite cells and/or incomplete recovery of the sutured or grafted nerves may be the cause of these discrepancies in the regeneration process.
Neuromuscular Disorders, 2006
Disuse induces skeletal muscle atrophy, but the molecular mechanism is largely unknown. In partic... more Disuse induces skeletal muscle atrophy, but the molecular mechanism is largely unknown. In particular, involvement of dystrophin glycoprotein complex (DGC), the main component of the sarcolemma, in disuse-induced muscle atrophy has not been fully examined. Twelve-week-old female C57BL/6 mice and neuronal nitric oxide synthase (nNOS)-null mice were randomly assigned to control or tail-suspension group. To induce muscle atrophy, the tail of the mouse was suspended from the top of the cage for 14 days. Skeletal muscles of the hind limbs were examined. We found that nNOS, a multifunctional regulator that is located at the sarcolemma as a member of DGC, quickly disappeared from the sarcolemma and was dislocated to the cytoplasm during tail suspension. Tail suspension-induced muscle atrophy was considerably relieved in nNOS-null mice. Furthermore, a nNOS-specific inhibitor significantly prevented suspension-induced muscle atrophy. nNOS can be a key molecule of molecular pathology of disuse-induced muscle atrophy. We, therefore, measured nitric oxide (NO) in skeletal muscle of living mice by using electron paramagnetic spectrometry and found that NO production was elevated in atrophied muscle, suggesting that NO is a possible mediator of muscle atrophy. Up-regulation of muscle atrophy-related E3 ubiquitin-ligases (MuRF-1 and Atrogin-1) and nuclear accumulation of de-phosphorylated Foxo3a were not evident in nNOS-null muscle after tail suspension. On the other hand, neither NFjB nor the Akt/S6k1/mTOR pathway is under the control of NO. The number of apoptotic myonuclei in tail-suspended nNOS-null mice was less than 20 % of that of tail-suspended wild-type mice. Glyceraldehyde-3-phosphate dehydrogenase (GAP-DH) was found to be nitrosated and removed to the nucleus in atrophied muscle together with an E3 ubiquitin-ligase, Siah-1. These findings strongly suggest that nitrosation of GAPDH by NO triggers apoptotic changes in myonuclei. In muscle biopsy specimens of neurogenic muscle atrophy such as amyotrophic lateral sclerosis, dislocation of nNOS was also observed in immunohistochemical study. We can conclude that dislocation of nNOS to the cytoplasm and overproduction of NO result in suspension-induced muscle atrophy. Pharmacological treatment to antagonize nNOS/NO can be a new therapeutic strategy to prevent muscle atrophy.