Decrease In Succinate Dehydrogenase Activity Research Articles

Cisplatin‐ and dietary ascorbic acid‐mediated changes in the mitochondria of Dalton’s lymphoma‐bearing mice

Cisplatin treatment caused a significant increase in the life span of ascites Dalton's lymphoma (DL) Tumor-bearing (TB) mice. However, as compared to cisplatin (CP) alone, combination treatment with ascorbic acid plus CP resulted in better therapeutic efficacy against murine DL. Cisplatin treatment of TB mice resulted in the appearance of thickened and irregular arrangement of mitochondrial cristae in the liver, kidney and DL tumor cells. Combination treatment of the hosts with ascorbic acid and CP lessened deformities in the mitochondria of liver and kidney, while in tumor cells, this increased the formation of vacuoles and disruption in mitochondrial cristae. Cisplatin treatment decreased the succinate dehydrogenase (SDH) activity in the mitochondria of kidney and DL cells and combination treatment caused further decrease in SDH activity in kidney and DL cells during 24-48 h of treatment. After CP treatment, the protein content in the mitochondria of these tissues decreased, and during combination treatment, it showed significant improvement. Mitochondrial lipid peroxidation (LPO) increased in these tissues after CP treatment. However, combination treatment significantly decreased mitochondrial LPO in liver and kidney but increased in DL cells. This increase in mitochondrial LPO in DL cells and decrease in liver and kidney could play an important role in the antitumor activity of combination treatment and at the same time reduce CP-induced toxicity in the host. However, further study may be desirable to explore some aspects of the mechanism(s) involved in these changes in mitochondria.

Structural and Functional Properties of an Upper Airway Dilator Muscle in Aged Obese Male Rats

Background: Age, obesity and male sex are risk factors for the development of obstructive sleep apnoea syndrome. Objective: We examined structural and functional properties of the sternohyoid muscle in young lean and aged obese male rats. We hypothesized that the aged muscle would be vulnerable to oxidative stress (hypoxia). Methods: Isometric contractile and endurance properties of the sternohyoid muscle were assessed in vitro with or without the superoxide scavenger Tempol (10 mM). Muscle fibre size and density were determined by myosin heavy chain immunofluorescence. Succinate dehydrogenase (SDH) and glycerol-3- phosphate dehydrogenase (GPDH) enzyme activities were determined. Results: Fibre hypertrophy, increased fast twitch (type 2X) fibre density, decreased SDH activity and increased GPDH activity, together with increased force and fatigue, were observed in aged obese muscles compared to young lean muscles. Tempol treatment increased strength and sensitivity to stimulation. Hypoxic depression of force was ameliorated by antioxidant treatment with equivalent effects in young lean and aged obese muscle. Conclusions: We conclude that the rat sternohyoid exhibits indefinite growth and is protected from oxidative stress as the animal ages.

Acclimation Induced Responses of SDH Activity of Tilapia (Oreochromis mossambicus) Following Introduction in a New Pond Habitat

Responses of the major mitochondrial respiratory enzyme succinate dehydrogenase (SDH) activity in gill and muscle tissue of tilapia (Oreochromis mossambicus) were investigated upon their transfer to a new pond habitat. Sixty healthy adult fish were procured from each of the three ponds used and were distributed in three cages in equal numbers; the cages were placed in each of the other two ponds as well as into original rearing pond. Four fish were removed from each cage every week and were sacrificed for the assay of SDH activity in gills and muscles. Transfer of fish from a stress condition to a benign environment and vice versa resulted in an increase and decrease in SDH activity of fish, respectively. The intensity of increase upon transfer was again dependent upon the amount of stress in the new habitat. In general, the SDH activity of the test fish strongly correlated with the ammonia concentration (P < 0.05) of water regardless of habitats. Time required for the introduced fish to acclimatize with new environmental conditions was dependent upon the environmental milieu of both its initial and final place of rearing and hence their physiological states. Differences in water quality, especially ammonia concentration, between its original place of rearing and the place of transfer were found to be responsible for the differences in acclimation period of two or three weeks. Relatively less difference in ammonia (2.68 for gills and 3.20 for muscles) between the initial place of rearing and new habitat resulted in acclimation of the fish one week earlier (second week) than the relatively wide difference (4.46 for gills and 5.62 for muscles) for third week. It may be reasonable to conclude that the varied responses of the mitochondrial respiratory enzyme of exogenously introduced fishes with the differences in the water quality—especially the ammonia concentration of ambient water between the original fish holding pond and growout pond—can be used to predict the time that will be required for the exogenously introduced fish to fully acclimatize with the new habitat.

Old mice present increased levels of succinate dehydrogenase activity and lower vulnerability to dyskinetic effects of 3-nitropropionic acid

Huntington's disease (HD) is a neurodegenerative disorder, with an age-related onset and a progressive development, characterized by choreiform movements. 3-Nitropropionic acid (3NP) induces the inhibition of succinate dehydrogenase (SDH), an increase in oxidative stress and anatomic changes that are related to the pathophysiology of HD. Hence, this toxin is a useful tool to study this pathology. This study compares the effects of 3NP on the development of orofacial dyskinesia (OD) and on SDH activity in young and old mice. Treatment with 3NP (5, 10, 15 or 20 mg/kg once a day, for four days) induced OD in young mice. Old mice presented an increase in the basal level of orofacial movement that was not potentiated by any dose of 3NP. Histochemical analyses showed that old mice presented an increase in the SDH activity. Finally, 3NP induced a decrease in SDH activity at both ages. We suggest that the 3NP-induced OD in young mice is related to the inhibition of SDH activity. In parallel, an enhancement in the basal activity of SDH could be related to the absence of a further increase in the OD presented by old mice treated with 3NP.

Cyclooxygenase inhibition attenuates 3‐nitropropionic acid‐induced neurotoxicity in rats: possible antioxidant mechanisms

Systemic administration of 3-nitropropionic acid (3-NP), a complex II inhibitor of the electron transport chain, causes motor and cognitive deficits that are associated with excitotoxicity and excessive free radical generation. Recently, cyclooxygenase (COX) inhibitors have been implicated as a neuroprotectant in the treatment of various neurological disorders. The present study was designed to investigate the effects of COX inhibitors in 3-NP-induced cognitive impairment and oxidative stress in rats. Intraperitoneal administration of 3-NP (20 mg/kg for 4 days) showed motor abnormalities and cognitive impairment in rats. Chronic treatment with naproxen (10 and 20 mg/kg) and valdecoxib (5 and 10 mg/kg) once daily for a period of 8 days beginning 4 days prior to 3-NP administration significantly improved 3-NP-induced motor and cognitive impairment in rats. Biochemical analysis revealed that systemic 3-NP administration significantly increased lipid peroxidation and nitrite levels, depleted reduced glutathione levels and reduced succinate dehydrogenase (SDH) activity in the brains of rats, whereas administration of naproxen, a nonselective COX inhibitor (10 and 20 mg/kg p.o.) and valdecoxib, a selective COX-2 inhibitor (5 and 10 mg/kg p.o.) significantly attenuated 3-NP-induced oxidative stress. Cyclooxygenase inhibitors also significantly restored the decreased SDH activity. The results of the present study clearly indicate that naproxen and valdecoxib showed protection against 3-NP-induced motor and cognitive impairment by decreasing oxidative stress.

Possible neuroprotective mechanisms of curcumin in attenuating 3-nitorpropionic acid-induced neurotoxicity

3-Nitropropionic acid (3-NP) is a well known fungic toxin causing neurotoxicity. Systemic administration of 3-NP causes motor and cognitive deficits that are associated with excessive free radical generation. Recently, curcumin has been implicated as a neuroprotectant in the treatment of various neurological disorders. The present study was designed to investigate the effects of curcumin in 3-NP-induced cognitive impairment and oxidative stress in rats. Curcumin, a potent antioxidant of dietary polyphenol, containing a standardized extract of Curcuma longa root (Zingiberaceae), has been reported to possess free radical scavenging, iron chelating and antiinflammatory activities. Intraperitoneal administration of 3-NP (20 mg/kg for 4 days) showed loss in body weight, declined motor function, poor retention of memory and changes in oxidative stress (lipid peroxidation, reduced glutathione and nitrite level) parameters in brain. Chronic treatment with curcumin (10, 20 and 50 mg/kg, p.o.) once daily for a period of 8 days beginning 4 days prior to 3-NP administration dose-dependently improved the 3-NP-induced motor and cognitive impairment. Biochemical analysis revealed that curcumin administration significantly attenuated 3-NP-induced oxidative stress (lipid peroxidation estimation, reduced glutathione and nitrite activity) in the brains of rats. It also significantly restored the decreased succinate dehydrogenase activity. The results of the present study clearly indicate that curcumin by its antioxidant activity showed neuroprotection against 3-NP-induced behavioral and biochemical alteration.

Effect of resveratrol on 3-nitropropionic acid-induced biochemical and behavioural changes: possible neuroprotective mechanisms

Huntington's disease is a progressive, degenerative disease characterized by abnormal body movements called chorea, and a reduction of various mental abilities. 3-Nitropropionic acid, an inhibitor of complex II of the electron transport chain, causes Huntington's disease-like symptoms in rodents. Recently, it has been reported that oxidative stress, which is one of the pathological hallmarks of various neurodegenerative disorders, also plays an important role in the pathogenesis of Huntington's disease. The present study was designed to investigate effects of resveratrol, an antioxidant with cyclooxygenase I inhibitory activity, in the 3-nitropropionic acid-induced model of Huntington's disease. Intraperitoneal administration of 3-nitropropionic acid (20 mg/kg for 4 days) caused significant loss of body weight, a decline in motor function (locomotor activity, movement pattern and vacuous chewing movements) and poor retention of memory. Repeated treatment with resveratrol (5 and 10 mg/kg, orally), once daily for a period of 8 days beginning 4 days prior to 3-nitropropionic acid administration, significantly improved the 3-nitropropionic acid-induced motor and cognitive impairment. Biochemical analysis revealed that systemic 3-nitropropionic acid administration significantly increased lipid peroxidation, nitrite levels, and depleted reduced glutathione levels, and decreased succinate dehydrogenase activity in the brains of rats. The results of the present study indicate that resveratrol (5 and 10 mg/kg, orally) significantly reversed 3-nitropropionic acid-induced motor and cognitive impairment, and that the beneficial effects of resveratrol might be attributed to its antioxidant activity.

Adaptive changes in the myocardium of patients with ischemic heart disease

Changes in the human heart muscle resulting from chronic coronary insufficiency have been analyzed using biopsies taken during surgery from nine patients with ischemic heart disease (IHD) and six patients with the WPW syndrome (without IHD). Histochemical analysis have shown that the atrial myocardium in IHD patients is characterized by an increased density of the microvascular network, increased phosphorylase activity, and decreased succinate dehydrogenase activity. Virtually the same changes have proved to occur in the myocardium of rats adapted to hypoxia by means of repeated exposure in a low-pressure chamber. According to the results of two-dimensional electrophoresis and immunoblotting, acid (but not alkaline) isoforms of inducible HSP70 proteins appear in the myocardium of IHD patients. It is concluded that the myocardium of IHD patients undergoes adaptive changes at the tissue level in response to repeated exposure to ischemia in the course of development of this disease. It is proposed that activation of the synthesis of alkaline HSP70 isoforms in the myocardium of cardiological patients may provide the possibility of improving its resistance to the impact of ischemia and reperfusion (this possibility is not realized under conditions of IHD).

Comparison of Cell Body Size and Oxidative Enzyme Activity in Motoneurons between the Cervical and Lumbar Segments in the Rat Spinal Cord after Spaceflight and Recovery

The cell body sizes and succinate dehydrogenase (SDH) activities of motoneurons in the dorsolateral region of the ventral horn at the cervical and lumbar segments in the rat spinal cord were determined following 9 days of spaceflight with or without 10 days of recovery on Earth. The motoneurons were divided into three types based on their cell body sizes; small-, medium-, and large-sized motoneurons. In control rats, there was no difference in the cell body size or SDH activity of small- and large-sized motoneurons between the cervical and lumbar segments. The SDH activity of medium-sized motoneurons in control rats was higher in the lumbar segment than in the cervical segment, while the cell body sizes of medium-sized motoneurons were identical. The SDH activity of medium-sized motoneurons in the lumbar segment decreased to a level similar to that in the cervical segment of control rats following spaceflight. In addition, the decreased SDH activity of medium-sized motoneurons persisted for at least 10 days of recovery on Earth. It is concluded that spaceflight selectively affects the SDH activity of medium-sized motoneurons in the lumbar segment of the spinal cord, which presumably innervate skeletal muscles having an antigravity function.

DYSTROPHIC CARDIOMYOPATHY IN PATIENTS WITH CHRONICAL VIRAL HEPATITIS

In patients with chronical viral hepatitis the earlier signs of myocardiodystrophy are nonspecific changes in ECG of the finite part of ventricular complex and I-type diastolic dysfunction of the left ventricle by Appleton. It has been detected that the decrease of Na+/T+-АТPase activity of erythrocytes along with the decrease of succinate dehydrogenase activity in peripheral blood lymphocytes is to be considered as an earlier pre-clinic sign of intracellular energy metabolism disturbance at dystrophic affection of myocardium.

Effect of glucocorticoids on 3-nitropropionic acid-induced oxidative stress in synaptosomes

The present study with rat striatal and cortical synaptosomes evaluated the effect of dexamethasone (300 μg/kg i.p./day) with and without simultaneous adrenalectomy on the oxidative stress induced by 3-nitropropionic acid (20 mg/kg/day for 4 days). Adrenalectomy enhanced the oxidative stress induced by 3-nitropropionic acid. These changes were prevented by previous and simultaneous administration of dexamethasone. Adrenalectomy alone induced oxidative stress with decreases in succinate dehydrogenase activity. Our results revealed that adrenal glucocorticoids, and especially dexamethasone (synthetic glucocorticoid), have a protective effect against oxidative stress induced by 3-nitropropionic acid in some brain regions of the Wistar rat.

Human and rat skeletal muscle adaptations to spinal cord injury.

Results of studies of rodent skeletal muscle plasticity are often extrapolated to humans. However, responses to "disuse" may be species specific, in part because of different inherent properties of anatomically similar muscles. Thus, this study quantified human and rat m. vastus lateralis (VL) fiber adaptations to 11 weeks of spinal cord injury (SCI). The m. VL was taken from 8 young (54 d) male Charles River rats after T-9 laminectomy (n = 4) or sham surgery (n = 4). In addition, the m. VL was biopsied in 7 able-bodied and in 7 SCI humans (31.3 +/- 4.7 years, mean +/- SE). Samples were sectioned and fibers were analyzed for type (I, IIa, IIb/x), cross-sectional area (CSA), succinate dehydrogenase (SDH), alpha-glycerol-phosphate dehydrogenase (GPDH), and actomyosin adenosine triphosphatase (qATPase) activities. Rat fibers had 1.5- to 2-fold greater SDH and GPDH activities while their fibers were 60% the size of those in humans. The most striking differences, however, were the absence of slow fibers in the rat and its four-fold greater proportion of IIb/x fibers (80% vs. 16% of the CSA) compared to humans. SCI decreased SDH activity more in rats whereas atrophy and IIa to IIb/x fiber shift occurred to a greater extent in humans. It is suggested that the rat is a reasonable model for studying the predominant response to SCI, atrophy. However, its high proportion of IIb/x fibers limits evaluation of the mechanical consequences of shifting to "faster" contractile machinery after SCI.

Effect of pyrethroids on carbohydrate metabolic pathways in common carp, Cyprinus carpio.

The activity levels of succinate dehydrogenase (SDH) and glucose-6-phosphate dehydrogenase (G6PD) were assessed in various tissues of Cyprinus carpio var communis which had been exposed to lethal concentrations of group-II pyrethroids (deltamethrin, cypermethrin, fenvalerate and fluvalinate) for a period of 72 h. The results indicated a steady decrease in SDH activity with a concomitant increase in G6PD activity. The decreased SDH activity indicated inhibition of SDH at mitochondrial level and the increased G6PD activity an enhancement of an alternative pathway of carbohydrate metabolism, viz the hexose monophosphate shunt (HMP) or pentose phosphate pathway as a biochemical adaptation to overcome the toxic stress.

Respiratory chain inhibition induces tolerance to focal cerebral ischemia.

The authors show that the inhibitor of the succinate dehydrogenase, 3-nitroproprionic acid (3-NPA), which in high doses and with chronic administration is a neurotoxin, can induce profound tolerance to focal cerebral ischemia in the rat when administered in a single dose (20 mg/kg) 3 days before ischemia. Infarcts were approximately 70% and 35% smaller in the 3-NPA preconditioned groups of permanent and transient focal cerebral ischemia, respectively. This regimen of 3-NPA preconditioning neither induced necrosis, apoptosis, or any other histologically detectable damage to the brain, nor did it affect behavior of the animals. 3-NPA led to an immediate (1-hour) and long-lasting (3-day) decrease in succinate dehydrogenase activity (30% reduction) throughout the brain, whereas only a short metabolic impairment occurred (ATP decrease of 35% within 30 minutes, recovery within 2 hours). The authors found that 3-NPA induces a burst of reactive oxygen species and the free radical scavenger dimethylthiourea, when administered shortly before the 3-NPA stimulus, completely blocked preconditioning. Inhibition of protein synthesis with cycloheximide given at the time of 3-NPA administration completely inhibited preconditioning. The authors were unsuccessful in showing upregulation of mRNA for the manganese superoxide dismutase, and did not detect increased activities of the copper-zinc and manganese superoxide dismutases, prototypical oxygen free radicals scavenging enzymes, after 3-NPA preconditioning. The authors conclude that it is possible to pharmacologically precondition the brain against focal cerebral ischemia, a strategy that may in principal have clinical relevance. The data show the relevance of protein synthesis for tolerance, and suggests that oxygen free radicals may be critical signals in preconditioning.

Local mitochondrial function following traumatic brain injury in rats.

The effect of lateral fluid percussion injury on mitochondrial function in the rat brain was investigated by quantitative imaging of changes in the regional activity of succinate dehydrogenase (SDH), a mitochondrial enzyme of the tricarboxylic acid cycle for adenosine triphosphate production. Regional SDH was measured in the frontal, parietal, temporal, and occipital cortices, CA1 and CA2-3 of the hippocampus, thalamus, corpus callosum, caudate/putamen, and cerebellum 1 hour and 72 hours after low, medium, and high pressure injury. No regional difference between the hemispheres in the activity of SDH was observed in the sham group. The hippocampus showed high SDH activity. The CA2-3 regions showed the highest activity among the regions examined. The corpus callosum, which is white matter, showed the lowest. One hour after low pressure fluid percussion injury, only the frontal lobe showed significantly lower SDH activity than the sham control in the ipsilateral hemisphere, whereas after 72 hours SDH activity was significantly lower in the frontal, parietal, and temporal lobes. SDH activity was significantly lower in the frontal, parietal, and temporal lobes in the medium and high pressure injury groups than in the sham control 1 hour after injury, and SDH activity in the CA1 and CA2-3 of the hippocampus was significantly decreased 72 hours after injury. No decrease in SDH activity was observed in any region of the contralateral hemisphere either 1 hour or 72 hours after injury. Mitochondrial dysfunction of the ipsilateral cortex and hippocampus following fluid percussion injury is correlated with the severity of injury and advances with time after injury. The results suggest that progression of mitochondrial dysfunction is associated with secondary bioenergetic deterioration.

Effect ofIn Vivo andIn Vitro treatment with arsenite on rat hepatic mitochondrial and microsomal enzymes

The effects of arsenite on activities of several enzymes including mitochondrial pyruvate dehydrogenase (PDH) and succinate dehydrogenase (SDH), microsomal cytochrome P450 and b5, NAD(P)H cytochrome C reductase and glutathione S-transferase were studied. The effects of arsenite on the mitochondrial membrane lipid peroxidation (LPO), the content of hepatic cytosol reduced glutathione and the activity of glutathione peroxidase was also investigated in rats. The results indicated that the activities of mitochondrial PDH and SDH were inhibited to 59 % and 57 % of the control activities respectively after arsenite was administered by intraperitoneal injection (i. p.) for 7 consecutive days at a dose of 20 mg/kg. Administration of arsenite led to a potential decrease of GSH content. The increase in lipid peroxidation of liver mitochondrial membrane prepared from rats treated with arsenite was also observed (P<0. 05). Arsenite did not appear to affect the liver cytosolic glutathione peroxidase and microsomal enzyme activitiesin vivo. Inin vitro test, liver mitochondria and cytosol were treated with arsenite, which led to a decreased SDH activity and GSH content and increase of mitochondrial LPO in a dose-dependent pattern that was similar to the results obtained inin vitro experiments. Selenite played a significant antagonistic role in effects of arsenite eitherin vivo orin vitro on the activities of mitochondrial PDH and SDH, and the content of mitochondrial LPO and cytosolic GSH. This results suggested that the toxic effects of arsenite on rat were associated with increased levels of LPO and the injured SH group in body caused by arsenite.

Hypoxia-dependent changes of enzyme activities in different fibre types of rat soleus and extensor digitorum longus muscles. A cytophotometrical study

Using cytophotometry activity changes of succinate dehydrogenase, glycerol-3-phosphate dehydrogenase and myofibrillar adenosine triphosphatase were measured in 3 fibre types of soleus and extensor digitorum longus muscles under normal and experimental conditions. Fibres were typed by means of cytophotometrical data into slow-oxidative, fast-oxidative glycolytic and fast-glycolytic ones. After experimental hypoxia of 20 min duration a significant increase of enzyme activities was observed especially in slow-oxidative and fast-oxidative glycolytic fibres of both muscles, e.g. succinate dehydrogenase activity increased by 21% in these fibres of soleus muscle and by 23-26% in these fibres of extensor digitorum longus muscle. Moreover, an increase of glycerol-3-phosphate dehydrogenase activity by 10% in slow-oxidative fibres and by 28% in fast-oxidative glycolytic fibres and a 10-12% increased ATPase activity in all fibres of extensor digitorum longus muscle were measured. Treatment with Ginkgo biloba extract for 3 months before exposure to hypoxia resulted in increased adenosine triphosphatase activity in all fibres of both muscles and in decreased succinate dehydrogenase activity of slow-oxidative and fast-oxidative glycolytic fibres of extensor digitorum longus muscle. These results could be interpreted as a protective effect of Ginkgo biloba extract.

Ultrastructural cytochemical analysis of cardiomyocytes in young and old rats subjected to general overheating

It is shown that regenerative plastic insufficiency develops in cardiomyocytes of young and old rats after a one-time general overheating. Atrophic and necrobiotic alterations of the cardiomyocytes together with a decrease of the heart weight are noted as well. Intracellular alterations of cardiomyocytes of young and old rats are accompanied by a marked decrease of succinate dehydrogenase activity under these conditions. There-after its activity rises appreciably in young animals during the course of postheating restitution, while in old rats the activity of this enzyme remains low.

Glutamate dehydrogenase in astrocytes of the rat dentate gyrus following lesion of the entorhinal cortex.

Applying quantitative microscopic histochemistry, the activity of the mitochondrial glutamate dehydrogenase which is localized in astrocytes was determined in the molecular layer of the dentate gyrus of the rat hippocampus. This hippocampal region contains the important terminations of the glutamatergic perforant path. For comparison, determinations of the mitochondrial succinate dehydrogenase were performed, which is localized preferentially in terminals and dendrites. Two age groups of animals were examined: young adults (three months old) and aged subjects (24 months old). Both age groups were divided into controls, and animals killed three, 21 and 90 days following unilateral electrolytic lesion of the entorhinal cortex. The post-lesional shrinkage of the terminal field of the perforant path, ipsilateral to the lesion side, was determined and considered in the evaluation of enzymatic data. Statistic analysis revealed that ipsilateral to the lesion side there was a significant decrease of glutamate and succinate dehydrogenase activities in the terminal field of the perforant path three, 21 and 90 days following lesion. It is reasonable to assume that the decrease of succinate dehydrogenase activity (50-60%) was caused by the loss of mitochondria localized in degenerating terminals, whereas the decrease of glutamate dehydrogenase activity (20-30%) was related to the decrease of glutamatergic transmission following lesion. In the terminal field of the perforant path contralateral to the lesion side both significant increases and decreases of enzyme activities were measured following lesion. From these results it is concluded that the hippocampus contralateral to the lesion side cannot be considered as an appropriate intraindividual control. The comparison between young and aged animals showed no differences in the demonstration of glutamate dehydrogenase and only restricted differences in the activity level of succinate dehydrogenase post-lesion. Therefore, it is reasonable to assume that the post-lesional reactivity of the enzymes studied was very similar in both age groups.

Activation-induced reduction of SDH activity in diaphragm muscle fibers

In this study, we examined whether exhaustive activation reduces succinate dehydrogenase (SDH) activity in diaphragm muscle fibers. In adult male rats (approximately 300 g), the costal diaphragm was excised and positioned in a chamber perfused with mammalian Ringer solution kept at 26 degrees C and oxygenated with 95% O2-5% CO2. The muscle was stimulated directly at 10 or 75 Hz in trains of 500 ms duration (1/s) for 8 min. An adjacent unstimulated segment of muscle served as control. The two muscle segments were frozen, and serial sections were stained for myofibrillar adenosinetriphosphatase activity after alkaline and acid preincubation to classify type I, IIa, and IIb fibers. The extent of glycogen utilization was also examined histochemically to confirm exhaustive activation of muscle fibers. SDH activity was quantified using a microdensitometric procedure implemented on an image-processing system. Exhaustive activation at both 10 and 75 Hz caused a significant decrease in SDH activity of all fiber types, with the decrease after 10-Hz stimulation being greater than that after 75-Hz stimulation. At both stimulation frequencies, type IIb fibers demonstrated the greatest decrease in SDH activity (36% after 10-Hz and 27% after 75-Hz stimulation), whereas type I and IIa fibers both displayed reductions of approximately 27 and approximately 19% after 10- and 75-Hz stimulation, respectively. The greater reduction of SDH activity in type IIb fibers indicates an inverse relationship between activation-induced reductions in SDH activity and fiber oxidative capacity.(ABSTRACT TRUNCATED AT 250 WORDS)