Increase In Serum Levels Of Enzymes Research Articles

Haematinic and Hepatoprotective Properties of Telfairia occidentalis Fruit Mesocarp on Phenylhydrazine-Induced Anaemia in Experimental Rats.

The level and potential of iron contained in fluted pumpkin (Telfairia occidentalis) has been exploited as a blood tonic; however, the potentials of some other parts of the plant are unknown. The effect of T. occidentalis fruit mesocarp (aqueous extract) on phenylhydrazine (PHZ)-induced anaemia in experimental rats was investigated in a bid to determine its curative properties and potential in reversing haemolytic anaemia and protection of liver health. The LD50 of the fruit extract was determined using Lorke's method for the determination of acute toxicity. The study involved oral administration of varying doses of the extract to different groups of rats which were monitored for 24 hours. The test sample did not show any signs of toxicity at doses of 5000 mg/kg b.wt, which is the highest possible recommended dose for toxicity testing. For the evaluation of the effects of the fruit extract on haematological indices and biochemical enzyme markers in anaemic rats, 30 matured albino Wistar rats were used. The rats were divided into five groups of six rats each. Group 1 consisted of normal rats (control group), Group 2 consisted of anaemic untreated rats, and Group 3 consisted of anaemic rats treated with the standard drug Astymin, while Groups 4 and 5 were made up of anaemic rats given the extract at doses of 600 mg/kg b.wt and 1000 mg/kg b.wt, respectively. The fruit extract failed to show any significant effect in improving the haemoglobin (Hb), alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphate (ALP) levels in anaemic rats but rather may have contributed to a reduction in Hb levels and an unhealthy increase in serum enzyme levels. This is indicative of the apparent inability of the aqueous extract of the T. occidentalis fruit mesocarp to reverse PHZ-induced haemolytic anaemia and may suggest a possible detrimental effect of high doses of the extract over a prolonged period.

Hepatoprotective Effect of Probiotic Lactic Acid Bacteria on Thioacetamide-Induced Liver Fibrosis in Rats

Hepatic fibrosis is a reversible wound-healing response characterized by the accumulation of extracellular matrix. Probiotics have been used to prevent and treat various disorders. The aim of the present study was to investigate the hepatoprotective effects of probiotic lactic acid bacteria (mixture of Lactobacillus paracasei, Lactobacillus casei, and Weissella confusa) on thioacetamide (TAA)-induced liver fibrosis in rats. Thirty-five male Wistar rats were randomly divided into five groups: (1) control, (2) TAA, (3) TAA+probiotics, (4) TAA+silymarin, and (5) probiotics. Group 1 rats received a standard diet. In groups 2-4, fibrosis was induced by intraperitoneal injection of TAA (200mg/kg BW) 3 times weekly for 8 consecutive weeks. Group 4 received TAA plus 100mg/kg BW of silymarin 2 times weekly. Groups 3 and 5 were fed 109CFU/mL viable microbial cells daily by gavage. The rats were sacrificed after 8weeks of treatment. Liver tissues were collected immediately and processed for histopathological, lipid peroxidation, and Western blot analyses of TNF-α, TGF-β1, and α-SMA. Blood serum was collected to measure liver enzymes. Rats in the TAA groups suffered from hepatic injury (increased serum enzyme levels, liver inflammation, and increased concentration of TNF-α, TGF-β1, and α-SMA proteins) and extensive liver fibrosis. In contrast, TAA-treated rats receiving probiotics or silymarin had significantly lower serum enzyme levels, less inflammation, and less fibrosis. Liver damage was lower in the TAA+probiotics-treated group. Consumption of a mixture of probiotic lactic acid bacteria attenuates the development of liver fibrosis.

Time Course and Association of Functional and Biochemical Markers in Severe Semitendinosus Damage Following Intensive Eccentric Leg Curls: Differences between and within Subjects.

Purpose: To investigate the extent and evolution of hamstring muscle damage caused by an intensive bout of eccentric leg curls (ELCs) by (1) assessing the time course and association of different indirect markers of muscle damage such as changes in the force-generating capacity (FGC), functional magnetic resonance (fMRI), and serum muscle enzyme levels and (2) analyzing differences in the degree of hamstring muscle damage between and within subjects (limb-to-limb comparison).Methods: Thirteen male participants performed six sets of 10 repetitions of an ELC with each leg. Before and at regular intervals over 7 days after the exercise, FGC was measured with maximal isometric voluntary contraction (MVC). Serum enzyme levels, fMRI transverse relaxation time (T2) and perceived muscle soreness were also assessed and compared against the FGC.Results: Two groups of subjects were identified according to the extent of hamstring muscle damage based on decreased FGC and increased serum enzyme levels: high responders (n = 10, severe muscle damage) and moderate responders (n = 3, moderate muscle damage). In the high responders, fMRI T2 analysis revealed that the semitendinosus (ST) muscle suffered severe damage in the three regions measured (proximal, middle, and distal). The biceps femoris short head (BFsh) muscle was also damaged and there were significant differences in the FGC within subjects in the high responders.Conclusion: FGC and serum enzyme levels measured in 10 of the subjects from the sample were consistent with severe muscle damage. However, the results showed a wide range of peak MVC reductions, reflecting different degrees of damage between subjects (high and moderate responders). fMRI analysis confirmed that the ST was the hamstring muscle most damaged by ELCs, with uniform T2 changes across all the measured sections of this muscle. During intensive ELCs, the ST muscle could suffer an anomalous recruitment pattern due to fatigue and damage, placing an excessive load on the BFsh and causing it to perform a synergistic compensation that leads to structural damage. Finally, T2 and MVC values did not correlate for the leg with the smaller FGC decrease in the hamstring muscles, suggesting that long-lasting increases in T2 signals after FGC markers have returned to baseline values might indicate an adaptive process rather than damage.

SIÇANLARDA KARBON TERAKLORÜR İLE UYARILMIŞ BEYİN HASARINDA Morus nigra’ NIN KORUYUCU MEKANİZMASI

Morus nigra (MN) is a common fruit used all over the world. Hepatic encephalopathy (HE) is a dangerous neuropsychiatric complication of both acute and chronic liver failure, and is the most common cause of death in patients with end-stage liver disease. To our knowledge, this is the first study investigated the efficiencies of MN on the treatment of HE on cirrhotic rat liver model induced by carbon tetrachloride (CCI 4 ) . I n this study it has been used superoxide dismutase ( SOD) and catalase (CAT) activities assays, 8-hydroxydeoxyguanosine (8-OHdG) immunohistochemistry and Haematoxylin-Eosin ( H&E ) staining in the brain, as well as aspartate aminotransferase ( AST) and alanine aminotransferase (ALT) levels in liver tissue With this aim, 42 Sprague-Dawley male rats were divided into six groups: control, HE control ( 1 mL/kg CCI 4 /twice a week, intraperitoneal ), 125 mg/kg MN , 250 mg/kg MN, CCI 4 +125 mg/kg MN and CCI 4 +250 mg/kg MN groups. CCl 4 caused a significant increase in serum enzyme levels in rat livers, compared with control. On the other hand, MN treatment restored the biochemical parameters significantly in a dose-dependent manner. 8-OHdG activity was significantly increased in CCI 4 group. However, these increases were significantly decreased by MN treatment. While intraperitoneal administration of MN significantly reduced oxidative stress, prevented apoptosis and caused an increase in the antioxidant defence mechanism activity in brain compared to the control group. B rains of rats treated with MN showed less DNA damage than treated groups with CCI 4 . As a result of t his study showed that MN has a neuroprotective effect because of its anti-inflammatory, anti-apoptotic, antioxidant properties.

A case of rhabdomyolysis related with low intensity body building exercise

Rhabdomyolysis is a clinical and biochemical syndrome resulting from the acute necrosis of muscle fibers and the leak of cellular elements into circulation. It can usually develop after trauma and severe exercises. However, it may also occur following low intensity exercises. In our case, a 24-year-old man was admitted to our emergency department because of severe abdominal pain after low intensity bodybuilding exercise. The development of an acute exertional rhabdomyolysis was confirmed by the increased serum enzyme levels. The patient was treated with intravenous sodium chloride, and sodium bicarbonate. In patients admitted to the emergency room after trauma or intensive exercise who are suspected of having rhabdomyolysis, the serum creatine phosphokinase, creatinine and potassium levels should be evaluated and if found to be high, fluid treatment should be started early to avoid any potential complications.

Diethylene glycol-induced toxicities show marked threshold dose response in rats

Diethylene glycol (DEG) exposure poses risks to human health because of widespread industrial use and accidental exposures from contaminated products. To enhance the understanding of the mechanistic role of metabolites in DEG toxicity, this study used a dose response paradigm to determine a rat model that would best mimic DEG exposure in humans. Wistar and Fischer-344 (F-344) rats were treated by oral gavage with 0, 2, 5, or 10g/kg DEG and blood, kidney and liver tissues were collected at 48h. Both rat strains treated with 10g/kg DEG had equivalent degrees of metabolic acidosis, renal toxicity (increased BUN and creatinine and cortical necrosis) and liver toxicity (increased serum enzyme levels, centrilobular necrosis and severe glycogen depletion). There was no liver or kidney toxicity at the lower DEG doses (2 and 5g/kg) regardless of strain, demonstrating a steep threshold dose response. Kidney diglycolic acid (DGA), the presumed nephrotoxic metabolite of DEG, was markedly elevated in both rat strains administered 10g/kg DEG, but no DGA was present at 2 or 5g/kg, asserting its necessary role in DEG-induced toxicity. These results indicate that mechanistically in order to produce toxicity, metabolism to and significant target organ accumulation of DGA are required and that both strains would be useful for DEG risk assessments.

The protective role of pomegranate juice against carbon tetrachloride–induced oxidative stress in rats

Most pomegranate (Punica granatum Linn., Punicaceae) fruit parts are known to possess enormous antioxidant activity. The present study was carried out to determine the phenolic and flavonoid contents of Derik pomegranate juice and determine its effect against carbon tetrachloride (CCl4)-induced toxicity in rats. Animals were divided into four groups (n=6): group I: control, group II: CCl4 (1ml/kg), group III: CCl4+pomegranate juice and group IV: CCl4+ursodeoxycholic acid (UDCA). Treatment duration was 4weeks, and the dose of CCl4 was administered once a week to groups II, III and IV during the experimental period. CCl4-treated rats caused a significant increase in serum enzyme levels, such as aspartate aminotransferase, alanine aminotransferase and total bilirubin, and decrease in albumin, when compared with control. Administration of CCl4 along with pomegranate juice or UDCA significantly reduces these changes. Analysis of lipid peroxide (LPO) levels by thiobarbutiric acid reaction showed a significant increase in liver, kidney and brain tissues of CCl4-treated rats. However, both pomegranate juice and UDCA prevented the increase in LPO level. Histopathological reports also revealed that there is a regenerative activity in the liver and kidney cells. Derik pomegranate juice showed to be hepatoprotective against CCl4-induced hepatic injury. In conclusion, present study reveals a biological evidence that supports the use of pomegranate juice in the treatment of chemical-induced hepatotoxicity.

Increased Serum Enzyme Levels Associated with Kupffer Cell Reduction with No Signs of Hepatic or Skeletal Muscle Injury

Macrophage colony-stimulating factor (M-CSF) is a hematopoietic growth factor that is responsible for the survival and proliferation of monocytes and the differentiation of monocytes into macrophages, including Kupffer cells (KCs) in the liver. KCs play an important role in the clearance of several serum enzymes, including aspartate aminotransferase and creatine kinase, that are typically elevated as a result of liver or skeletal muscle injury. We used three distinct animal models to investigate the hypothesis that increases in the levels of serum enzymes can be the result of decreases in KCs in the apparent absence of hepatic or skeletal muscle injury. Specifically, neutralizing M-CSF activity via a novel human monoclonal antibody reduced the CD14(+)CD16(+) monocyte population, depleted KCs, and increased aspartate aminotransferase and creatine kinase serum enzyme levels in cynomolgus macaques. In addition, the treatment of rats with clodronate liposomes depleted KCs and led to increased serum enzyme levels, again without evidence of tissue injury. Finally, in the osteopetrotic (Csf1(op)/Csf1(op)) mice lacking functional M-CSF and having reduced levels of KCs, the levels of serum enzymes are higher than in wild-type littermates. Together, these findings support a mechanism for increases in serum enzyme levels through M-CSF regulation of tissue macrophage homeostasis without concomitant histopathological changes in either the hepatic or skeletal system.

The detection and significance of serum enzymes in the adult with central nervous system infections

Objective To study the serum enzyme in the adult central nervous system infection in patients and its clinical significance,aimed at providing basis for the diagnosis and prognosis of the adult central nervous system infection. Methods 68 patients with central nervous system infections were treated in June 2008 to Decem 2009 in Neurology Department of our hospital. In addition, 60 healthy persons were selected at the same time as control group. Serum aspartate aminotransferase ( AST), lactate dehydrogenase ( LDH) , Creatine kinase ( CK) , CK-MB ( CK-MB)levels were detected. Results AST,LDH,CK and CK-MB levels of the central nervous system infection group were higher than the control group,and the difference between the two groups was statistically significant(P<0.05). Severe group AST, LDH, CK and CK-MB and other content of the four enzymes were higher, and the difference between the two groups is also significant ( P < 0.05 ). Conclusions Adult patients with central nervous system infection significantly increased serum enzyme levels, and serum enzyme levels had a positive correlation with the severity. Serum enzyme was a reliable adult central nervous system infections diagnostic index. Key words: Central nervous system infections; Aspartate aminotransferases; L-lactate dehydrogenase; Creatine kinase

Protective effects of coumarin and coumarin derivatives against carbon tetrachloride-induced acute hepatotoxicity in rats

The comparison of the antioxidant activity of some coumarins with their molecular structure is well determined. However, the protective function of coumarins with various chemical structures against liver toxicity has not yet been well established. Therefore, the aim of this study was to evaluate the possible cytoprotective properties of coumarin and some coumarin derivatives against CCl 4 (carbon tetrachloride)-induced hepatotoxicity. Coumarin (1,2-benzopyrone) and coumarin derivatives esculetin (6,7-dihydroxycoumarin), scoparone (6,7-dimethoxycoumarin) and 4-methylumbelliferone (7-hyroxy-4-methyl) were examined for their protective effect against CCl 4-induced hepatotoxicity in Male Sprague-Dawley rats. A single toxic dose of CCl 4 (1.25 ml kg −1, orally) produced liver damage in rats, seen histologically as centrilobular necrosis. Administration of CCl 4 increased serum enzyme levels of aspartate transaminase (AST), alanine transaminase (ALT), and alkaline phosphatase (ALP). Pre-treatment of rats with esculetin (31.15 mg kg −1, orally) and scoparone (35 mg kg −1, orally) significantly prevented CCl 4-induced increase in serum enzymes, whereas 4-methylumbelliferone (35 mg kg −1) and coumarin (30 mg kg −1) had no effect against CCl 4-induced rise in serum enzymes. Morphological findings were consistent with the plasma transaminase observations. Among the coumarin analogs, esculetin, which possesses orthodihydroxy coumarins, showed the strongest protective effect against CCl 4-induced liver damage, followed by scoparone, 4-methylumbelliferone and coumarin, respectively. The results of this study indicate that the chemical structures of coumarins play an important role in the prevention of liver toxicity.

Low-intensity body building exercise induced rhabdomyolysis: a case report

IntroductionRhabdomyolysis is a severe and debilitating condition that promotes muscle breakdown and is a relatively rare, not always diagnosed cause of acute renal failure (ARF) with an 8–20% reported incidence. Exertional rhabdomyolysis only appears in adult patients 24–48 h after strenuous activities as military basic training, weight lifting, and marathon running.Case presentationA 30-year-old man was admitted to our department because of weakness and painful swelling of the muscles as well as dark urine appearing 24 h after carrying out a body-building exercises of low intensity. The development of an acute exertional rhabdomyolysis was confirmed by the increased serum enzyme levels and myoglobinuria. The patient was treated with intravenous sodium chloride, and sodium bicarbonate. The nephrotoxicity of myoglobin was decreased by forced alkaline diuresis.ConclusionThe reported case emphasizes the occurrence of acute rhabdomyolysis even in those who underwent a low-intensity exercise. A proper treatment is mandatory to avoid a sudden worsening of clinical conditions eventually evolving to acute renal failure.

A Study On The Acute Toxicological Effects Of Commercial Diesel Fuel In Nigeria In Rats (Ratus ratus.) Using Hematological Parameters

The acute toxicology effect of diesel fuel in rats using hematological parameters was investigated. Five groups of rats consisting of ten rats per group, all of 0.2kg average body weight were used for the study. Four doses (65/kg; 87 g/kg; 209; g/kg; 131 g/kg) of diesel fuel were administered intraperitoneally, into the rats and the effect monitored within 24hours. The following hematological parameters ( Haemoglobin concentration, palled cell volume, white blood cell count) and enzyme (Aspartate/ alamine aminotransferases and alkaline phosphatase) levels were monitored. Results indicated a decrease in haemoglobin concentration, packed cell volume and white blood cell count with increase in dose levels of diesel fuel in the rates. Conversely, there was an increase in serum enzyme levels with increase in dose of diesel fuel. The results indicate possible aplastic anaemia in the rat being in the rats being induced by administration of diesel fuel. Furthermore, the enzyme analysis results suggested a possible hepatotoxic effect of diesel fuel in the rat. (Journal of Applied Sciences & Environmental Management: 2002 6(1): 84-86)

Targeting of Liposomal Flavonoid to Liver in Combating Hepatocellular Oxidative Damage

The efficacy of mannosylated liposome formulations with Quercetin (QC, a flavonoid antioxidant isolated from indigenous origin) has been tested in vivo against carbon tetrachloride(CCl 4) -induced liver oxidative damage in rats. Single subcutaneous injection of CCl 4 (40% v/v in olive oil; 1 ml/kg) induces the generation of toxic oxygen radicals and results in hepatocellular damage. The increased serum enzyme levels (glutamate pyruvate transaminase, alkaline phosphatase) and hepatocellular conjugated diene levels by CCl 4 induction were significantly lowered due to pretreatment with mannosylated liposomal QC (MLQ) (0.5 ml liposomal suspension containing 0.27 mg QC), whereas the same amount of free QC was found to be ineffective. In addition, the effectiveness of MLQ on CCl 4 -induced acute liver damage also was evaluated by tissue histopathological examination. Damage produced by CCl 4 in liver reverted to normal with pretreatment of MLQ.

Screening of antioxidant action of various molds and protection of Monascus anka against experimentally induced liver injuries of rats

Antioxidant action of various molds, which are traditionally used for the production of foods or alcoholic beverages in Japan, was studied in vitro and in vivo. Antioxidant action was evaluated by scavenging stable free radical 1,1-diphenyl-2-picrylhydrazyl (DPPH) and lipid peroxidation of rat liver microsomes. Among 40 molds, 16 species showed the DPPH scavenging action, and the molds that can scavenge the DPPH radical inhibited lipid peroxidation. The mold with the strongest action, Monascus anka, was chosen for the investigation of a protective action against liver injury of rats. When galactosamine (GalN, 400 mg/kg) or GalN plus lipopolysaccharide (LPS, 0.5 μg/kg) was given intraperitoneally to rats (Sprague-Dawley), aspartate aminotransferase (AST) and glutathione (GSH) S-transferase (GST) activities in serum were significantly increased. However, such hepatotoxicities seen in the increase in serum enzyme levels were depressed when the extract prepared from M. anka was given 1 and 15 h before the toxic insultant. Liver microsomal GST activity, which is known to be activated by oxidative stress, was increased by GalN or GalN plus LPS treatment and the increase was also inhibited by pretreatment with the extract. Pathomorphological changes in the liver caused by GalN treatment also were prevented by the mold extract. These results indicate that the extract of M. anka has radical scavenging action and ameliorates chemically induced hepatotoxicity.

Effects of Repeat Dosing and Multiple Blood Drawing Separately and Together on Carbon Tetrachloride–Induced Hepatotoxicity

A series of experiments was conducted to assess the effects of prior dosing and/or multiple modest blood withdrawal on subsequent carbon tetrachloride (CCl4)-induced hepatotoxicity. Adult male Wistar rats were randomly assigned to the following treatments: oil-CCl4, oil-bleed-CCl4, CCl4-CCl4, and CCl4-bleed-CCl4, with bleed groups having 1 ml of blood removed at baseline (time 0), 24, 48, 72, and 120 h. At these times the levels of serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) were determined. The serum enzyme levels of the CCl4 (0.9 ml/kg, vol/vol in corn oil, per os) treated rats (treated at time 0) had returned to untreated levels prior to the administration of the second dose (120 h). Serum enzyme (AST/ALT) levels were measured again 24 and 48 h after the second CCl4 (0.9 ml/kg, 1:1 vol/vol in corn oil, per os) treatment. The results indicated that the prior dose of CCl4 (0.9 ml/kg, 1:1 vol/vol in corn oil, per os) enhanced the hepatotoxicity of a subsequent identical dose of CCl4 three- to six-fold when the two doses were separated by 2–14 days, although the prior dose was protective when administered 24 h before the second dose. Prior multiple blood drawing also enhanced the hepatotoxicity of a subsequent dose of CCl4 (0.9 ml/kg, 1:1 vol/vol in corn oil, per os) three-fold. The effect of blood drawing has been demonstrated to cross sex and strain when tested on male and female Sprague-Dawley and Wistar rats. The combination of the two procedures (with the two CCl4 doses separated by 5 days) enhanced the hepatotoxicity of a subsequent identical dose of CCl4 (0.9 ml/kg, 1:1 vol/vol in corn oil, per os) 10-fold. Subsequent sham bleed experiments indicated that the increase in serum enzyme levels previously associated with blood withdrawal is substantially associated with the handling (i.e. stress) involved in blood withdrawal rather than the removal of modest amounts of blood per se.

An infarct-like myocardial lesion experimentally induced in Wistar rats with Africanized bee venom.

There is evidence in the literature that death following a bee or wasp sting may result from cardiac involvement. This study describes acute cardiac lesions experimentally induced in Wistar Rats submitted to intravenous inoculation of Africanized bee venom (ABV) and killed 1, 4, and 24 h after inoculation. Significant increases in serum enzyme levels were detected; light microscopy showed necrosis of the myocardium; and enzyme histochemistry showed inactivation of enzymes in and around the areas of necrosis. This is the first report of an acute necrotizing cardiac lesion, similar to human myocardial infarction, produced by the inoculation of ABV.

Hepatoprotective activity of carrot ( Daucus carota L.) against carbon tetrachloride intoxication in mouse liver

The effect of carrot extract on carbon tetrachloride (CCl 4)-induced acute liver damage was evaluated. The increased serum enzyme levels (viz., glutamate oxaloacetate transaminase, glutamate pyruvate transaminase, lactate dehydrogenase, alkaline phosphatase, sorbitol and glutamate dehydrogenase) by CCl 4-induction were significantly lowered due to pretreatment with the extract. The extract also decreased the elevated serum bilirubin and urea content due to CCl 4 administration. Increased activities of hepatic 5′-nucleotidase, acid phosphatase, acid ribonuclease and decreased levels of succinic dehydrogenase, glucose-6-phosphatase and cytochrome P-450 produced by CCl 4 were reversed by the extract in a dose-responsive way. Results of this study revealed that carrot could afford a significant protective action in the alleviation of CCl 4-induced hepatocellular injury.

Effect of antioxidant treatment in rats with acute hemorrhagic pancreatitis

The purpose of this study was to evaluate the effect of free radical ablation therapy in acute hemorrhagic pancreatitis. Acute pancreatitis was induced in 64 rats by retrograde injection of 5% sodium taurocholate. Thirty animals were pretreated with 100,000 units/kg/hr of superoxide dismutase (SOD) and 400,000 units/kg catalase within the first 3 hr. After 0.5, 3.5, and 12 hr of observation time, serum enzymes and the tissue content of conjugated dienes, malondialdehyde, reduced and oxidized glutathione, as well as ATP, ADP and AMP were measured. In addition, tissue samples were examined by light microscopy. Untreated rats (N = 34) developed within 12 hr an acute hemorrhagic necrotizing pancreatitis with a concomitant increase in serum enzyme levels and a decrease in reduced glutathione and ATP. Within the 12-hr observation period, 57% of the animals died. Scavenger treatment improved the tissue damage and attenuated the increase of the serum enzyme levels and the decrease in reduced glutathione and ATP. Moreover, the lethality rate was significantly lower. Oxygen radicals seem to be instrumental for the development of acute hemorrhagic pancreatitis. Thereby, antioxidant treatment reduces tissue damage, biochemical alterations and extrapancreatic complications, thus improving the final outcome.

Identification of a homozygous missense mutation (Arg to Gly) in the critical binding region of the human EC-SOD gene (SOD3) and its association with dramatically increased serum enzyme levels.

Journal Article Identification of a homozygous missense mutation (Arg to Gly) in the critical binding region of the human EC-SOD gene (SOD3) and its association with dramatically increased serum enzyme levels Get access Rodney J. Folz, Rodney J. Folz * 1Department of Medicine Duke University Medical CenterDurham, NC 27710, USA * To whom correspondence should be addressed Search for other works by this author on: Oxford Academic PubMed Google Scholar Laura Peno-Green, Laura Peno-Green 1Department of Medicine Duke University Medical CenterDurham, NC 27710, USA Search for other works by this author on: Oxford Academic PubMed Google Scholar James D. Crapo James D. Crapo 1Department of Medicine Duke University Medical CenterDurham, NC 27710, USA2Department of Pathology, Duke University Medical CenterDurham, NC 27710, USA Search for other works by this author on: Oxford Academic PubMed Google Scholar Human Molecular Genetics, Volume 3, Issue 12, December 1994, Pages 2251–2254, https://doi.org/10.1093/hmg/3.12.2251 Published: 01 December 1994 Article history Received: 02 August 1994 Accepted: 07 October 1994 Published: 01 December 1994

The Macroenzymes: A Clinical Review

Macroenzymes are serum enzymes that have a higher molecular mass than the corresponding enzyme normally found in serum under physiologic or pathophysiologic conditions. Although no evidence convincingly indicates that macroenzymes cause disease or necessitate treatment, some patients with immunoglobulin-complexed enzyme disorders have previously been reported to have associated autoimmune diseases or malignant lesions. To address this issue, we reviewed the medical records of 42 patients in whom a macroenzyme had been detected during assessment at the Mayo Clinic between 1986 and 1990. Of these 42 patients, 21 had macro-creatine kinase, 10 had macro-lactate dehydrogenase, 6 had macro-aspartate aminotransferase, and 5 had macroamylase in the serum. Although the study group did not include all Mayo patients with this phenomenon, it represented a sufficient sample size to determine retrospectively whether specific dismissal diagnoses were present concurrently. The most common findings in this group of patients with macroenzymes were (1) advanced age (except for those with macro-aspartate aminotransferase), (2) cardiovascular disease (probably due to sampling bias), (3) malignant lesions (particularly in those with macro-creatine kinase), and (4) rheumatologic disease (in those with macro-lactate dehydrogenase). The immunoglobulin-complexed enzyme disorders are characterized by increased total serum enzyme levels that are often isolated and persistent. Physicians should be aware of the presence of macroenzymes so that invasive or costly procedures are not undertaken unnecessarily to determine the cause of increased serum enzyme levels.