Development of a two-channel system for monitoring the mirror elements of the Millimetron space observatory.

The paper presents the results of the development of an onboard two-stage telescope monitoring (control) system of the Millimetron space observatory. A 3D laser scanner is used for the preliminary inspection of the reflector elements, and an image analyzer based on the Foucault knife method is used for the final one. The results of the calculation and modeling of the monitoring system for tuning the telescope elements into space are presented. The signals formed in the system are calculated, including using data on the actual shape of the manufactured mirror elements. Estimates of the expected measurement accuracy are given, and the test results of the developed system are presented.

[Experimental evidence of magnesium salts for treatment of calcium oxalate nephrolithiasis in an animal model based on sodium oxalate and a cyclooxygenase 2 selective inhibitor].

The purpose of present study was to investigate influence of magnesium (Mg) salts (Mg L-aspartate, Mg chloride) and their combinations with pyridoxine on development of calcium-oxalate nephrolithiasis induced by sodium oxalate (3% diet weight) and celecoxib (100 mg per kg of bodyweight) according to B.C. Jeong et al. (Urol. Res. 2005; 33(6): 453-459). On 14th day of diet urinary oxalate level and crystalluria were significantly increased, creatinine clearance tended to be lower as compared to control group. Mg L-aspartate, Mg chloride and their combinations with pyridoxine, MagneB6 (Mg lactate in combination with pyridoxine) and Mg sulfate were given by intragastric intubation from 15th till 28th days of diet (50 mg Mg per kg body weight). On 28th day urinary oxalate level in rats treated with Mg salts was lower by in average 45%, creatinine clearance was increased by 19%, Ca/Mg ratio decreased by 1.5-2 times in comparison with animals fed with diet alone. Light microscopic examination of kidney sections have revealed decreased inclusion volume fraction of renal calcification in rats treated with Mg salts as to compare with untreated rats receiving sodium oxalate and celecoxib (0.3-1.0% vs. 4%). So, Mg salts prevented development of calcium-oxalate nephrolithiasis in hyperoxaluric rats. Morphological and laboratory tests showed Mg aspartate and magne B6 were more effective Mg-containing substances in comparison with other studied salts.

[The effectiveness of certain magnesium salts in nephrolithiasis caused by the use of sodium oxalate and celecoxib].

The study was aimed to evaluation the effect of different magnesium salts and their combinations with pyridoxine on a course of calcium-oxalate nephrolithiasis, which was modeled by adding the sodium oxalate (3% of weight of the diet) and selective cyclooxygenase-2 inhibitor celecoxib at a dose 100 mg/kg body weight to a diet for 4 weeks. Starting from the 2nd week of the experiment, the animals had received one of the following compounds: magnesium L-aspartate, magnesium chloride, and their combination with vitamin B6; magnesium sulfate and Magne B6 (magnesium lactate and vitamin B6) as comparators. 28 days after the start of the experiment, disorders progressed in the group receiving only celecoxib and oxalate-rich diet: the urine level of oxalate increased by 171% (p < 0,0001), crystalluria had increased (up to 105 crystals in 10 microml of urinary sediment, p < 0,0001), creatinine clearance decreased by 29%, compared to control (p = 0,087). Increasing calcium/magnesium and oxalate/creatinine ratios in urine by 16 and 189%, respectively, was observed. In the renal parenchyma of animals treated with sodium oxalate and celebrex, calcifications with a volume fraction of 4% were identified, whereas these changes were absent in intact animals. According to the degree of correction ofhyperoxaluria and elimination of calcium oxalate crystals, investigated salts showed similar efficacy, with the exception of magnesium sulfate, which less contributed the compensation of abnormalities in kidney and urinary. According to the data of morphological study, the volume fraction of calcifications was lowest in the groups receiving magnesium L-aspartate and Magne B6.

[Effects of magnesium salts on the course of experimental calcium-oxalate urolithiasis].

Experimental urolithiasis was induced in 80 white non-inbred male rats by adding 0.75% ethylene glycol and 2% ammonium chloride to drinking water by Fan et al. After significant differences in crystalluria, oxaluria and urine pH were achieved in hyperoxaluric rats vs controls one, hyperoxaluric rats were given magnesium (Mg) salts Mg chloride, Mg L-aspartate either alone or in combination with pyridoxine hydrochloride (B6) in comparison with Mg sulfate and magne B6 (mg lactate in combination with B6) in a dose of 50 mg of elementary Mg per 1 kg of body weight. All the rats were fed with Mg-adequate diet containing 0.84 g of Mg oxide (0.5 g of elementary Mg per kg of diet). Calcium-oxalate urolithiasis has developed in rats taking ethylene glycol and ammonium chloride for 28 days. An urinary oxalates levels increased threefold, oxalate/creatinine--fourfold. Calcium oxalate crystals were detected in the urine of rats drinking solution of ethylene glycol and ammonium chloride, pH decreased by 20%, fractional excretion (FE) of Mg increased by 60%, FE of phosphate--by 58.2%, FE of calcium--by 95.8%, creatinine clearance lowered by 39.2% in comparison with intact group. Magnesium salts administration resulted in reduction of urine oxalates, crystalluria, phosphate excretion, Ca/Mg and oxalate/creatinine ratios, increased urine pH and creatinine clearance. Mg L-aspartate in combination with vitamin B6 appeared the most effective salt and significantly more effective than magnesium sulfate.

Correction of furosemide-induced magnesium deficiency with different stereoisomers of organic magnesium salts: a comparative study.

We compared the efficiency of different stereoisomers of organic magnesium salts (Mg DL-, Mg D-, and Mg L-aspartate and Mg L- and Mg DL-glutamate) after oral administration under conditions of furosemide-induced magnesium deficiency. The time to complete compensation of erythrocyte magnesium level was 5 days for Mg L-aspartate, 10 and 8 days for Mg L-glutamate and Mg D-aspartate, respectively, and 11 days for Mg DL-aspartate and Mg DL-glutamate. These findings attest to better bioavailability of Mg complex with L-stereoisomer of aspartate in comparison with DL and D-stereoisomers and stereoisomers of Mg glutamate.

[Pharmacological correction of pain sensitivity threshold in magnesium deficiency].

The purpose of this study was to compare effect of: Mg L-aspartate and MgCl2 alone and in combination with pyridoxine (B6) on hyperalgesia in rats fed with Mg-deficient diet. To induce hypomagnesemia, two hundred rats were placed on a Mg-deficient diet (MP Biomedicals Inc., OH) and demineralized water. To evaluate pain sensitivity, motor and vocalization threshold in response to a mechanical stimulus (Randall-Selitto paw pressure test) and tail withdrawal, simple and brief vocalization threshold in response to an electrical stimulation (algesimetry by electrical stimulation of the tail through intracutaneous needles) were assessed. In our study Mg deficiency results in reduced vocalization threshold by 42% in response to a mechanical stimulus. Thresholds of motor tail response, simple vocalization and brief vocalization after discharge in response to an electrical stimulation were decreased by 32.5%, 20.5% and 23.8%. Oral magnesium salts led to normalization of thresholds of pain sensitivity with a return to pre-deficient levels. Magnesium salts in combinations with pyridoxine tended to be significantly more effective in Randall-Selitto paw pressure test as compared with salts without pyridoxine. The effect of studied salts was comparable with those observed in Magne B6 treatment and significantly higher than in magnesium sulfate treatment.

[Comparative study of magnesium salts bioavailability in rats fed a magnesium-deficient diet].

The purpose of this study was to compare efficiency of compensation of alimentary Mg deficiency after administration of 12 organic and 8 inorganic magnesium salts and to evaluate the ability of vitamin B6 to accelerate their effect. Two hundred eighty rats were placed on a Mg-deficient diet (Mg content (15 mg/kg) and demineralized water for 7 weeks. Twelve control rats were fed a basal diet (Mg content 500 mg/kg). Starting from day 49 of the Mg-deficient diet, the rats were given magnesium salts (50 mg magnesium and 5 mg pyridoxine per kg): Mg chloride, Mg sulphate, Mg oxide, M nitrate, Mg thiosulphate, Mg hydrophosphate, Mg carbonate, Mg trisilicate, Mg (L-, D- and DL-) aspartate, Mg (L- and DL-) pyroglutamate, Mg succinate, Mg glycinate, Mg orotate, Mg taurate, Mg lactate or their combination with vitamin B6 (5 mg/kg b.w.). Erythrocyte and plasma Mg levels were measured by spectrophotometry following the colour reaction between Mg and titanium yellow. Mg L-aspartate compensated for magnesium deficit more effectively and faster than all other salts. Mg chloride showed the highest efficiency among inorganic magnesium salts. Both Mg chloride and Mg L-aspartate in combination with vitamin B6 caused statistically significant compensation of magnesium deficit.

[Effects of mangesium salts and their combinations with vitamin B6 on oxalates crystalluria in rats fed with pyridoxine-deficient diet].

We studied the effects of oral magnesium (Mg) salts either alone or in combination with pyridoxine hydrochloride in rats on pyridoxine-deficient diet. Fifty-four male rats were randomized into two groups and were fed either a standard diet or a pyridoxine-deficient diet for 3 weeks. A significant rise of the EGOT index ( > 1.5), oxaluria (from 74.8 +/- 5.2 to 117.9 +/- 12.3 mcM/l, p = 0.035), and crystalluria in rats fed with pyridoxine deficient diet were revealed. Oral Mg chloride, Mg L-aspartate either alone or in combination with pyridoxine in comparison with magnesium sulfate, magne B6 (Mg lactate with pyridoxine) and pyridoxine alone were administered (50 mg of magnesium and/or 5 mg of pyridoxine per kg body weight). Magnesium salts in combination with pyridoxine lowered an oxalate level and crystalluria whereas magnesium salts alone reduced only crystalluria. Antilithis effects of Mg L-aspartate and Mg chloride in combination with pyridoxine were comparable with those observed in magne B6 or pyridoxine treatment and were significantly higher than in magnesium sulfate treatment.

Features of central neurotransmission in animals in conditions of dietary magnesium deficiency and after its correction.

Magnesium is important in the regulation of neurotransmitter metabolism and the modulation of receptor function in the CNS, including neurotransmitters and receptors involved in the pathogenesis of many mental disorders. The aim of the present work was to perform a pharmacological evaluation of the central mechanisms of action of magnesium salts in the clofelin, phenamine, arecoline, nicotine, apomorphine, and 5-hydroxytryptophan tests in conditions of dietary magnesium deficiency. After reaching the magnesium deficiency state, animals were given oral (via tube) magnesium L-asparaginate and magnesium chloride lone and in combination with vitamin B(6), as well as the reference agent Magne B6. Our assessments of phenamine stereotypy in magnesium-deficient animals showed reductions in the latent period by an average of 14.89% and a significant increase in the duration of phenamine stereotypy by an average of 19.44% (from 268.23 +/- 8.17 to 320.36 +/- 19.90 min) as compared with intact rats. Studies of hyperkinesia induced by 5-hydroxytryptophan showed a two-fold reduction in its extent in the magnesium-deficient group (p

[Depression-like and anxiety-related behaviour of rats fed with magnesium-deficient diet].

The aims of this study were to estimate of psychomotor activity, emotional status and magnesium (Mg) content in blood of rats fed with Mg-deficient diet for 49 days; and to find out whether the combination of vitamin B6 with Mg will reveal antidepressant- and anxiolytic-like activity and reduce the length of the treatment needed to recover rats from Mg-deficient condition. To induce hypomagnesemia, seventy-nine rats were placed on a Mg-deficient diet (Mg content < or = 15 mg/kg) and demineralized water for 7 weeks. Eight control rats were fed a basal control diet. On the forty-ninth day of Mg-deficient diet, rats were treated one of the six supplementations: Mg L-aspartate alone and in combination with pyridoxine, MgCl2 x 6H2O alone and in combination with pyridoxine, Magne B6 (Mg lactate with pyridoxine) and Mg sulfate (50 mg Mg and 5 mg vitamin B6 per kg). In our study Mg-deficiency was associated with depleted intraerythrocytic (0.748 +/- 0.036 vs. 1.83 +/- 0.026 mmol/l, p < 0.001) and plasma (0.567 +/- 0.029 vs. 1.20 +/- 0.030 mmol/l, p < 0.001) Mg level compared to control rats. It was shown Mg deficiency resulted in depression-like and anxiety-related behavior in rats. Open field test result in rats including locomotor activity (number of crossed squares) and vertical activity (number of standing on hind paws), number of visiting in central squares were decreased significantly. In the elevated plus maze test, the number of visiting open arms (by 63.6%) and residence time (by 78.5%) of rats were significantly less as compared with the control group. In the forced swimming test, time immobile was significantly increased (by 70.2%) and time of swimming was decreased (by 15%) compared to control. Mg salts alone and in combination with vitamin B6 administered to Mg-deficient rats increased the Mg level in plasma and erythrocytes. Furthermore, this increase was in relation to vitamin B6 given to the animal. It was established, that the application of Mg L-aspartate and MgCl2 x 6H2O in combinations with pyridoxine led to correction of behavioural disturbances of Mg-deficient animals. Antidepressant- and anxiolytic-like activity of studied salts was comparable with those observed in Magne B6 treatment and significantly higher than in Mg sulfate treatment.

[The characterization of central neuromediation in rats fed with magnesium-deprived diet before and after magnesium replenishment].

Magnesium (Mg) has been proposed to take part in biochemical dysregulation contributing to psychiatric disorders. The aims of this study was to estimate acute behavioural responses to clonidine (0.1 mg/kg i.p.), d-amphetamine (5 mg/kg, i.p), arecoline (15 mg/kg i.p), nicotine (6 mg/kg i.p.), apomorphine (1.5 mg/kg i.p.) and L-5-hydroxytryptophan (300 mg/kg i.p.) in rats fed with Mg-deprivated diet for 49 days and then treated with organic and inorganic Mg salts (50 mg Mg per kg) ether alone or in combination with pyridoxine (5 mg vitamin B6 per kg). In our study Mg-deficient rats were more sensitive to d-amphetamine-induced motor stereotypes compared with control rats; time of onset of the stereotypies insignificantly decreased by 14.89% and duration of the stereotypies significantly increased by 19.44% (320.36 +/- 19.90 vs. 268.23 +/- 8.17 minutes; p = 0.043). Mg deficiency did not modulate sensitivity to nicotine-induced seizure. The time between nicotine injection and emergence of clonic seizure (seizure latency) in the controls and Mg-deficient rats were 0.80 +/- 0.26 and 0.96 +/- 0.21 minutes respectively. Duration of the seizures in the controls and Mg-deficient rats were 64.93 +/- 7.20 and 79.32 +/- 8.13 minutes. In our study, Mg deficiency did not affect on clonidine- and apomorphine-induced hypothermia. Clonidine produced similar decreases in rectal temperature in controls and Mg-deficient group. In experiments using apomorphine, values of hypothermia were similar to those observed with clonidine. Mg deficiency antagonized 5-hydroxytryptophan-induced head-twitch response. The number of head twitches produced by 5-hydroxytryptophan was significantly (p = 0.49) decreased: twofold in magnesium-deficient rats (1.23 +/- 0.44 per minute) as compared with controls (2.42 +/- 0.52 per minute). Arecoline-induced tremor was comparably less expressed in Mg-deficient rats than in controls. The time between arecoline injection and time of onset of the tremor in the controls and Mg-deficient rats were 92.75 +/- 19.35 and 245.17 +/- 121.86 seconds respectively (p < or = 0.035). Duration of the tremors in the controls and Mg-deficient rats were 1175.58 +/- 127.87 and 703.83 +/- 89.33 seconds (p = 0.015). Magnesium salts (Mg chloride, Mg L-aspartate alone and in combination with B6) were administered through gastric tube during twenty days up to complete compensation oferythrocyte and plasma Mg levels in all experimental groups. In our study administration of Mg salts resulted in normalization of acute behavioural responses in Mg-deficient rats to d-amphetamine, arecoline, and L-5-hydroxytryptophan. Behavioural responses in rats treated with both Mg chloride and Mg L-aspartate in combinations with B6 were comparable with those observed in MagneB6 treatment.

[Effect of some organic and inorganic magnesium salts on lipoprotein state in rats fed with magnesium-deficient diet].

Low serum magnesium (Mg) concentrations have been reported in patients with atherosclerosis. From the other hand numerous clinical reports suggest the beneficial effects of Mg adjuvant therapy for the treatment of atherosclerosis. The purpose of this present study was to compare the effect of Mg L-aspartate and Mg chloride alone and in combinations with pyridoxine, Mg sulfate and Magne B6 (Mg lactate with pyridoxine) on lipid profile in rats fed with Mg deficient diet. To induce hypomagnesemia, fifty-three rats were placed on a Mg-deficient diet (ICN Biomedicals Inc. Aurora, OH) and demineralized water for 7 weeks. Seven control rats were fed a basal control diet (Mg content = 500 mg/kg) and water (with Mg content 20 mg/l) for equal duration. On the forty-ninth day of Mg-deficient diet, rats were treated one of the six supplementations: Mg chloride, Mg L-aspartate alone and in combinations with pyridoxine, Mg sulphate and Magne B6 (50 mg Mg and 5 mg vitamin B6 per kg). In our study Mg deficiency resulted in increase of triglyceride (by 35.2 %p < 0.0001), LDL (more than fourfold p < 0.0001), total cholesterol (by 38.7% p < 0.0001), apolipoprotein B (by 74.1%, p = 0.0006) levels and decrease in concentration of HDL (by 28.7% p < 0.0001). The non-HDL cholesterol/HDL cholesterol ratio was more than threefold increased (p < 0.0001). Oral magnesium salts led to normalization of lipid state with a return to pre-deficient levels. Magnesium salts in combinations with pyridoxine tended to be significantly more effective as compared with salts without pyridoxine. The hypolipidemic effect of studied salts was comparable with those observed in Magne B6 treatment and significantly higher than in magnesium sulfate treatment.

[The role of alimentary magnesium deficiency in development of nephrolithiasis and its correction with magnesium salts in rats].

Aims of our work were to appraise the quantity and nature of renal calcifications and mineral metabolism in the magnesium-deficient rats; and to find out whether the combination of pyridoxine with Mg L-aspartate or Mg chloride will reduce the length of the treatment needed to recover rats from magnesium deficient condition and urolithiasis state. To induce hypomagnesemia, fifty rats were placed on a magnesium-deficient diet (magnesium content < or = 15 mg/kg) and demineralized water for 10 weeks. On the forty-ninth day of magnesium-deficient diet, rats were treated one of the six supplementations: MgCl2, Mg-L-Asp or their combinations with pyridoxine hydrochloride, magnesium sulfate, magne B6.

[Study of anti-inflammatory activity of some organic and inorganic magnesium salts in rats fed with magnesium-deficient diet].

The purpose of the present research was comparative study of anti-inflammatory action of some Mg salts in rats fed with Mg-deficient diet. It was shown in our study that administration of Mg L-aspartate with pyridoxine leads to higher compensation of Mg deficiency in rats with diet-induced Mg depletion as compared with other Mg supplementations. According to the Mg deficiency correction rate Mg salts may be ranged in the following order: Mg L-aspartate with pyridoxine > or = Mg chloride with pyridoxine > or = Mg lactate with pyridoxine > or = Mg L-aspartate > Mg chloride > Mg orotate. In our study administration of Mg salts resulted in decreased number of blood leukocytes, reduced peripheral vasodilation visible in the external ear, decreased spleen weight, and as consequences in reduced inflammatory and immunological response. According to correction rate of the inflammatory response Mg salts may be ranged in the following order: Mg orotate > or = Mg chloride > or = Mg chloride with pyridoxine > or = Mg L-aspartate > or = MgL-aspartate with pyridoxine > or = Mg lactate with pyridoxine.

Effect of magnesium chloride and magnesium L-aspartate on seizure threshold in rats under conditions of dietary magnesium deficiency.

We studied the effect of Mg-L-aspartate, MgCL2, and their combinations with vitamin B6, magneB6, and MgSO4 on seizure threshold in rats with dietary Mg2+ deficiency. Mg2+ deficiency was followed by a decrease in the threshold dose of corazol (from 79.20 to 49.48 mg/kg), shortening of the latency of the first jerk (by 33.6%, p=0.012), and reduction of the time to the first episode of clonic seizures (by 32.6%, p=0.011). Seizure threshold and latencies of the first jerk and first episode of clonic seizures increased over 3 weeks after peroral administration of Mg2+ salts. The combination of Mg2+ salts and pyridoxine was most effective in this respect.

[Changes in myocardium, skeletal muscle and liver of rats fed carnitine-deficient diet and treated with carnitine optical isomers].

The aim of the present study was a comparative assessment of L-, D-and DL-carnitine effect on morphometric and histological parameters of myocardium, skeletal muscles (m. gastrocnemius) and liver in 60 rats fed carnitine-deficient diet. Carnitine-deficient diet fed 2 months resulted in a substantial reduction of carnitine concentration in blood plasma of rats. In carnitine-deficient animals, lipid vacuoles were found to accumulate within the hepatocytes in all the zones of hepatic lobules, which mainly had the character of micro- and macrovesicular steatosis. This was accompanied by a reduction of skeletal muscle fiber and cardiomyocyte average thickness. L-carnitine administration resulted in the compensation of carnitine deficiency in animals with alimentary carnitine deficient state, while the racemate and D-stereoisomere did not affect its content in blood. Pharmacological correction of carnitine deficiency with L-carnitine prevented the development of liver fatty dystrophy to a greater degree, than the administration of other carnitine stereoisomeres and promoted the restoration of muscular fiber thickness of skeletal muscles. DL-carnitine administration was accompanied by a moderate correction of fatty dystrophy and did not prevent the development of skeletal muscles atrophy. D-carnitine stereoisomere did not prevent liver fatty dystrophy, but it reduced its severity. Correction of carnitine deficiency with D- stereoisomere was not accompanied by essential morphological and morphometric differences in degree of skeletal muscle atrophy.

[Comparative evaluation of the effects of carnitine stereoisomers and racemate on the cardio- and hemodynamics of rats on a carnitine-deficient diet].

L-carnitine (L-beta-hydroxy-gamma-N,N,N-trimethylaminobutyric acid) is conditionally necessary for mitochondrial transport and metabolism of long-chain fatty acids, and thus for myocardial energetic metabolism. D-carnitine is not biologically active and might interfere with proper utilization of the L isomer, and so there are claims that the racemic mixture (DL-carnitine) should be avoided. The pharmacological effects of carnitine are stereospecific: L-carnitine was effective in various animal and clinical studies, while D- and DL-carnitine was found to be ineffective or even toxic to some cells and tissues, such as muscle cells and the myocardium. DL-carnitine caused symptoms of myasthenia and cardiac arrhythmias, which disappeared after L-carnitine administration. Therefore, the purposes of this work were (1) to study the effect of L-carnitine vs. that of D- and DL-stereoisomers on carnitine restoration rate in blood plasma of carnitine-deficient rats and (2) to evaluate the effect of stereoisomers and racemate of carnitine on the cardio- and hemodynamics of rats on carnitine-deficient diet. To induce carnitine deficiency, 60 rats were placed on a carnitine-deficient diet containing 1 g of N-trimethyl-hydrazine-3-propionate (mildronate) per a kilogram of the diet. The controls, 15 rats, received a basal control diet of the same duration. After 80 days, L-, D-, and DL-carnitine were administered in a dose of 200 mg/kg per os for 30 days, together with the carnitine-deficiency diet. To investigate the effect of L-, D-, and DL-carnitine on the abnormalities of the myocardial function of the carnitine-deficiency rats, various hemodynamic variables including left ventricular pressure, indices of contractility and relaxation, heart rate, systolic and diastolic blood pressure in response to volume loading test, adrenoreactivity test, and maximal isometric loading test, were measured. In this study, the carnitine-deficient diet with mildronate caused a substantial loss of carnitine in blood plasma by 56.49% (19.70 +/- 4.97 vs. 45.27 +/- 6.97 micromol/ 1, p < 0.001), which was accompanied by myocardial malfunctioning. After 30 days of L-carnitine administration, the plasma level of carnitine was significantly higher by an average of 118.55% (p < 0.001) compared with carnitine-deficient controls, while after administration of D- and DL-stereoisomers the carnitine content did not change or increased insignificantly. L-carnitine administration to carnitine-deficient rats led to normalization in myocardial function including indices of contractility and relaxation, systolic and diastolic blood pressure in response to volume loading test, adrenoreactivity test, and maximal isometric loading test. Chronic administration of D- and DL-carnitine did not change an altered cardio- and hemodynamics of carnitine-deficient rats compared with L-carnitine.

Effects of L-, D-, and DL-carnitine on morphometric parameters of skeletal muscle and exercise performance of laboratory animals receiving carnitine-deficient diet.

Serum concentration of L-carnitine, the mean thickness of the skeletal muscle fiber, and exercise performance in the forced swimming test decreased in rats receiving a carnitine-deficient diet. Treatment with L-carnitine compensated for carnitine deficiency, while racemate and D-stereoisomer did not increase its level. L-Carnitine, but not racemate and D-stereoisomer, promoted recovery of the skeletal muscle fiber thickness and exercise performance of rats.