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PubMed1984

Transaminase elevations in patients receiving bovine or porcine heparin.

Eighty-six patients who required heparin therapy were randomly assigned to receive bovine or porcine heparin. Abnormal concentrations of alanine transaminase and aspartate transaminase developed during treatment in 59.3% and 26.7% of patients, respectively. Patient characteristics that significantly influenced the development of abnormal alanine transaminase concentrations were male sex and higher baseline enzyme values. Transaminase concentrations returned to normal in 80% of patients after heparin therapy was discontinued and in 20% during therapy. Analysis of transaminase concentrations in all 86 patients showed that 95% had some increase in enzymes during treatment. Mean maximal increase over baseline for all patients was 3.6 for alanine transaminase and 3.1 for aspartate transaminase (range, 1.0 to 15). Lactate dehydrogenase concentrations became abnormal in 35.7% of patients. Lactate dehydrogenase isoenzyme determinations in 6 patients showed elevated hepatic fractions. No clinical symptoms of hepatic dysfunction were seen.

Adolescent↗

PubMed1993

Heparin-induced transaminase elevations: a prospective study.

An intensive and prospective surveillance study of 54 patients hospitalized in the Internal Medicine Unit of Clinical Hospital of the Catholic University of Chile, who required heparin in the period between June and December of 1991 was done. The aim of the work was to characterize and study the incidence of the adverse reactions associated with heparin therapy, with special emphasis on abnormal serum transaminase elevation. Abnormal transaminase elevation was defined as a rise over 20% of the serum transaminase baseline value. For determining the serum transaminase level, a UV spectrophotometric method was used. The incidence of the adverse drug reactions (ADR) was 24.1% (13 ADR), 8 of which (14.8%) were related with heparin therapy. Three of them (5.5%) corresponded to alanine transaminase (ALAT) increase and five (9.3%) to aspartate transaminase (ASAT) elevation. By means of global introspection method, 3 cases of ALAT increases were defined as probable and 6 as possible, while 5 ASAT increases were estimated as probable and 14 as possible. All of them were of slow onset, did not require treatment and hospital stay was not prolonged. Two patients' characteristics--age and sex--were associated with the development of heparin-induced abnormal alanine transaminase concentrations. The younger male patients showed a greater frequency of heparin-induced ALAT elevation. However, this association was not observed with the heparin-induced ASAT increase. These reactions were dose-dependent. Patients with heparin-induced ALAT elevation received a dose of 154,220 IU +/- 72,970 IU in comparison to patients without that adverse reaction who received 96,210 IU +/- 40,340 IU. This difference was statistically significant.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1989

Inhibition of rat liver transaminases by low levels of acetaldehyde and the pharmacologic effects of B6 vitamers.

To better define the significance and mechanism of acetaldehyde-mediated transaminase inhibition, acetaldehyde metabolism was studied in rat liver homogenates and cytosols. When either preparation was incubated at 37 degrees with 1.5 mM acetaldehyde for 4 hr, acetaldehyde levels fell rapidly in the first 30 min and little inhibition of aspartate aminotransferase (GOT) or alanine aminotransferase (GPT) resulted. In contrast, incubation with 50 mM ethanol also resulted in a peak acetaldehyde level of 1.0 to 1.5 mM by 2 hr, but this level was then maintained for the next 2 hr and transaminases were inhibited by 20-35%. Sequential addition of low dose (125-250 microM) pulses of acetaldehyde to rat liver preparations resulted in a progressive decrease in the rate of acetaldehyde disappearance. When the pulsing schedule was adjusted accordingly to maintain acetaldehyde levels between 50 and 250 microM for 8 hr, transaminases were again inhibited by 20-40%. Finally, addition of 1-5 mM pyridoxal and pyridoxal 5'-phosphate, aldehydic B6 vitamers, to cytosols 2-4 hr after pulsing with acetaldehyde was begun, almost completely prevented further transaminase inhibition. In contrast, the non-aldehydic B6 vitamers, pyridoxine, pyridoxamine and pyridoxamine 5'-phosphate, did not affect acetaldehyde-mediated transaminase inhibition. These findings suggest that (1) prolonged exposure to low levels of acetaldehyde impairs acetaldehyde metabolism in rat liver homogenates and cytosols; (2) acetaldehyde toxicity may be more dependent on sustained exposure to acetaldehyde than on the peak level of acetaldehyde attained; and (3) aldehydic B6 vitamers can modify on-going acetaldehyde-mediated transaminase inhibition.

Acetaldehyde↗

PubMed2001

Circulating E-selectin levels in chronic hepatitis C patients with normal or elevated transaminase before and after alpha-interferon treatment.

E-selectin, an adhesion molecule of the selectin family, is involved in leukocyte adhesion to the endothelium and in the cellular immunological reactions. Expression of this molecule, in fact, is physiologically absent, but it becomes evident on sinusoidal lining cells during inflammatory liver disease. The aim of this study was to evaluate the behavior of E-selectin in chronic hepatitis C (CH-C) patients with persistently normal transaminase in comparison to patients with CH-C and elevated transaminase, and its changes during alpha-interferon therapy. Immunohistochemical localization of E-selectin was also performed on liver tissue specimens of both groups. Fifty-eight subjects were divided into 3 groups: group A included 18 patients with CH-C and persistently normal transaminase; group B 20 patients with CH-C and persistently elevated transaminase levels and group C included 20 healthy subjects, representing the control group. The first two groups were treated with r-IFN alpha at a dose of 6 MU 3 times a week for 3 months and followed-up with 3 MU 3 times a week for another 3 months. Serum baseline values of E-selectin in groups A and B were significantly higher than those in group C (P < 0.04), but there was no difference between groups A and B. Furthermore, there was a trend toward higher E-selectin values as histological severity increased (r = 0.69; P < 0.0001). Post-treatment E-selectin serum values showed a moderate decrease in both groups, but only among responder patients; while E-selectin levels were unchanged in non responders. Immunohistochemical localization showed no staining for E-selectin in normal liver specimens, while there was a quite similar staining for E-selectin in the two groups of patients. In conclusion, this study shows that serum E-selectin levels in patients with CH-C and persistently normal transaminase are higher than in controls and they are associated with severity of liver disease. Liver of these patients express E-selectin molecules, suggesting an activation of the immune system almost identical to that of patients with CH-C and elevated transaminase. In both groups only responder patients showed a moderate decrease below baseline serum values.

Adult↗

PubMed2001

Clinical significance of elevated serum interferon- inducible protein-10 levels in hepatitis C virus carriers with persistently normal serum transaminase levels.

The aim of this study was to assess the immunological profile in hepatitis C virus carriers with persistently normal serum transaminase levels. Forty-two serum HCV RNA positive patients with persistently normal serum transaminase levels (22 natural 'asymptomatic HCV carriers' and 20 biochemical responders to IFN therapy) and 23 complete responders to IFN therapy were enrolled. The HCV genotypes and serum HCV RNA levels were determined before IFN therapy in treatment responders, and at entry in the others. The serum levels of IFN-inducible protein-10 (IP-10) (a protein mainly induced by IFN-gamma), interleukin (IL)-10, and IL-4 were measured in all patients while the serum transaminase levels were normal. The serum transaminase levels and platelet counts were then monitored for the next 4 years and the changes in liver fibrosis were assessed. The serum levels of IP-10 in infected and biochemically normal patients were significantly higher than the levels in complete responders to therapy, whereas the serum levels of IL-10 and IL-4 did not vary significantly among the different groups. During the 4-year follow-up period, 10/20 (50%) biochemical responders and 12/22 (55%) asymptomatic carriers had an elevation of the serum transaminase levels. A significant (P=0.0370) increase in platelet count after 4 years and improvement in liver fibrosis were noted in treatment responders but not in infected patients. The weak but significant residual immune response as reflected by the increased serum IP-10 level may underlie the outcome of HCV carriers with persistently normal serum transaminase levels.

Alanine Transaminase↗

PubMed2006

A novel pattern of transaminase elevation associated with autologous transplant for neuroblastoma.

To determine the pattern and degree of hepatic transaminitis experienced by children undergoing autologous transplantation for neuroblastoma. Sixty-four children with high-risk neuroblastoma received an autologous transplant with cyclophosphamide, etoposide, and carboplatin conditioning. Forty-eight went on to receive a second transplant with M and TBI conditioning. Charts were reviewed for evidence of hepatic regimen-related toxicity. A high rate of transaminitis was observed after both regimens. In each transplant, there was an early period of transaminitis during conditioning, from which patients recovered, followed by a second period of transaminase elevation. The degree of elevation was not associated with age, whether the administered dose was calculated based on a per kg or per M(2) basis or the presence of regimen-related severe mucositis. Elevated transaminases at admission were not associated with maximal hepatotoxicity during the first transplant although there was an association in the second transplant. However, the magnitude of transaminase elevation was less in the second transplant. VOD occurred in one and three patients in transplants 1 and 2, respectively. Both conditioning regimens were associated with an early and late elevation of transaminases without significant cholestasis. This biphasic pattern of transaminitis has not been reported previously. The high prevalence of transaminase elevation at time of both transplants was not associated with an increased incidence of VOD. We conclude that elevated transaminases should not preclude proceeding to a first or second autologous transplant with these regimens.

Antineoplastic Combined Chemotherapy Protocols↗

PubMed1975

Modulation of leucine transaminase activity by dietary means.

The specific activity of leucine transaminase was measured in supernatants of liver, skeletal muscle (gastrocnemius), and kidney homogenates obtained from fed, starved, and protein-deprived rats. After 12 h of starvation, there were slight reductions in leucine transaminase activity of both muscle and kidney tissues. When starvation was prolonged to 1 full day, the activity of this enzyme increased by approximately twofold in both muscle and kidney. Prolongation of fasting to 5 days resulted in an additional increase in specific activity of leucine transaminase in muscle. During the entire 5 days of starvation, leucine transaminase activity remained unaltered in liver of starved rats. Protein deprivation for 1 or 5 days resulted in significant reductions in specific activity of leucine transaminase in skeletal muscle. Protein deprivation did not produce a remarkable effect on the activity of this enzyme in kidney or liver tissue. The results of this study, together with those previously obtained, indicate that within our experimental conditions increased oxidation of leucine in skeletal muscle of starved rats is not initially related to an alteration in activity of leucine transaminase. When caloric deficiency is prolonged, the potential for transamination is also increased. These adaptive changes increase the ability of skeletal muscle to use leucine as a metabolic fuel.

Animals↗

PubMed1991

Molecular cloning of the L-phenylalanine transaminase gene from Paracoccus denitrificans in Escherichia coli K-12.

The L-phenylalanine transaminase gene of Paracoccus denitrificans was cloned by a shotgun method using the Escherichia coli K-12 mutant DG30, which lacks three distinct transaminase genes. Plasmid pPAP142 was constructed by inserting a 2.2-kb fragment carrying the transaminase gene into pUC18. Strain E. coli K-12 HB101 cells harboring the plasmid produced 20-fold to 30-fold more transaminase than wild type P. denitrificans cells. The nucleotide sequence of the 2.2-kb fragment was determined, revealing that the deduced amino acid sequence of the transaminase of P. denitrificans is similar to that of other transaminases.

Amino Acid Sequence↗

PubMed1981

Laboratory assessment of severe chronic active liver disease during and after corticosteroid therapy: correlation of serum transaminase and gamma globulin levels with histologic features.

Serum glutamic oxaloacetic transaminase and gamma globulin levels were correlated with morphologic findings during and after corticosteroid therapy of severe chronic active liver disease to assess ability to monitor histologic change. Morphologic features were interpreted by a single observer from 441 coded biopsy specimens obtained from 69 patients. Serum glutamic oxaloacetic transaminase values were more predictive of histologic findings than gamma globulin levels (p less than 0.02), correctly reflecting morphologic status in 67% of instances during treatment and 80% after treatment. Abnormalities in either test identified chronic active liver disease with similar accuracy, but serum glutamic oxaloacetic transaminase determinations were more sensitive to active inflammation. Serum glutamic oxaloacetic transaminase elevations of more than twice normal during and after therapy were reliably associated with chronic active liver disease. Normal laboratory studies, however, did not detect chronic active liver disease in 55% of cases during treatment and 19% after therapy. The majority of lesions undetected by laboratory investigations comprised periportal necrosis while confluent necrosis was rarely missed. We conclude that serum glutamic oxaloacetic transaminase determinations provide a useful mechanism for monitoring chronic active liver disease. During therapy, serum glutamic oxaloacetic transaminase levels reliably discount resolution, but do not predict histologic inactivity. After treatment, laboratory surveillance inconsistently detects periportal necrosis, but rarely misses severe inflammation of potentially greater prognostic significance.

Adrenal Cortex Hormones↗

PubMed1994

[Significance of elevated transaminase levels at the end of pregnancy].

During normal pregnancy, serum transaminase levels remain within normal limits. An elevated level observed in a pregnant woman always signals a disease process, most often of hepatic origin, but in certain cases, of muscular origin. During the last three months of pregnancy and in the immediate post partum period a large number of liver diseases can cause elevated transaminase levels, depending upon the clinical presentation. In everyday practice, a complete liver battery together with specialized consultation is required for all pregnant women with raised transaminase levels. Toxaemia gravis may be evident in patients with severely raised blood pressure, especially if seizures occur. Epigastric or subcostal pain should suggest hepatic involvement. Hypertension may however be absent and epigastric or left shoulder pain may be the only clinical signs. Acute liver steatosis is 20 to 50 times more rare than toxaemia and may cause nausea and vomiting. Certain non-specific signs such as asthenia, anorexia, polyalgia, abdominal pain, diarrhoea and fever, together with pruritus should suggest acute hepatitis. A 25-fold increase in transaminase level is commonly encountered. The risk of fulminating hepatitis is less than 1/1000 but should always be entertained. All drugs should be stopped and careful research for recent xenobiotic contamination (drugs, infusions, alphamethyldopa, etc.) should be undertaken. Viral hepatitis requires serovaccination of the newborn at birth. Herpetic hepatitis is rare but requires rapid diagnosis (liver biopsy) and treatment with acyclovir in addition to cesarean section and treatment of the newborn at birth. Rare cases of hepatitis E may occur after a stay in North Africa, the Middle-East, Southeast Asia or Mexico. Chronic cases with or without temporary pruritus suggest infectious hepatitis B or C although, in chronic hepatitis C, serum transaminase levels often return to normal during pregnancy. Rare cases of asymptomatic elevations of serum transaminase levels can reveal subclinical chronic hepatitis.

Acute Disease↗

PubMed1964

RADIOSENSITIVITY OF SEVERAL DEHYDROGENASES AND TRANSAMINASES DURING SPOROGENESIS OF BACILLUS SUBTILIS.

Rowley, D. B. (Syracuse University, Syracuse, N.Y.), and H. R. Newcomb. Radiosensitivity of several dehydrogenases and transaminases during sporogenesis of Bacillus subtilis. J. Bacteriol. 87:701-709. 1964.-Cells of Bacillus subtilis grown in a chemically defined medium for 17 hr, subsequently washed, and transferred to a phosphate solution containing CaCl(2) sporulated in a reproducible pattern. The synthesis of dipicolinic acid essentially paralleled the appearance of thermoresistant cells. X-ray resistant cells appeared 2 to 3 hr before the appearance of thermoresistant cells and the formation of dipicolinic acid. Changes in enzyme activity of cells undergoing sporogenesis varied among the enzymes studied. The transaminases exhibited a marked decrease in activity during early sporogenesis, whereas the dehydrogenases exhibited maximal activity. The determination of enzyme radioresistance in extracts of sporulating cells indicated that the resistance of transaminases remained essentially unchanged, whereas the dehydrogenases exhibited a decreased resistance early in sporogenesis. Although both glutamic-pyruvic transaminase and glutamic-oxaloacetic transaminase (GOT) were demonstrated in vegetative cells, only the latter was detected in mature spores. The radioresistance of GOT in vegetative-cell extracts was two to three times greater than in spore extracts.

Alanine Transaminase↗

PubMed1991

Transaminases changes and worm burden in multiple infection of Ancylostoma caninum in mice.

Aspartate transaminase level was significantly increased in intestine of experimentals that received multiple doses of infection. The level of alanine transaminase rose to a significant value in liver of mice infected with multiple doses. Rise of transaminases is correlated with the necrosis (disruption of intestina) hepatic cells in infected mice. Changes and/or the distribution of aspartate transaminase and alanine transaminase with regard to the dosage is discussed.

Alanine Transaminase↗

PubMed1987

Serum transaminase levels and cholescintigraphic abnormalities in acute biliary tract obstruction.

Twenty-five patients presenting to the hospital with symptoms suggestive of acute biliary tract disease were noted to have a characteristic pattern of transaminase and cholescintigraphic abnormalities. There was marked variability in the initial serum transaminase levels; however, 16 patients had aspartate aminotransferase levels greater than 300 IU, and 19 patients had alanine aminotransferase values greater than 300 IU. Regardless of the initial values, there was a 76% (aspartate aminotransferase) and 58% (alanine aminotransferase) reduction in transaminase levels within 72 hours, prior to therapeutic relief of bile duct obstruction. In ten patients with common bile duct obstruction, cholescintigraphy revealed no excretion of technetium Tc-99m-labeled iminodiacetic acid, for up to two hours after injection, into the extrahepatic biliary tract or small bowel. Common bile duct stones were present in 16 patients, five patients had acute pancreatitis, and four patients were thought to have spontaneously passed common duct stones. We believe that high transaminase levels may be found in patients with obstructive biliary tract disease, sequential measurements of transaminase levels may provide an important diagnostic clue for biliary tract disease, and nonexcretion of radionuclide on cholescintigraphy may be a feature of acute bile duct obstruction.

Acute Disease↗

PubMed1979

Similarities between cysteinesulphinate transaminase and aspartate aminotransferase.

A method for the purification of two cysteinesulphinate transaminases, A and B (EC 2.6.1), is described. These enzymes catalyse the conversion of cysteinesulphinic acid to beta-sulphinyl pyruvate. The final preparations are homogeneous by polyacrylamide gel electrophoresis, sodium dodecyl sulphate-polyacrylamide gel electrophoresis and isoelectrofocusing. The molecular weight of the subunits is 41 000 for cysteinesulphinate transaminase A and 43 400 for B. Both enzymes are unspecific, as L-asparate, L-glutamate and L-cysteic acid serve as substrates in addition to L-cysteinesulphinic acid. Cysteinesulphinate transaminase A has a Km of 9.8 mM for cysteinesulphinic acid and 0.25 mM for aspartic acid, whereas the B enzyme has a Km of 6.5 mM for cysteinesulphinic acid and 1.4 mM for aspartic acid. The Vmax values of the A and B enzymes are respectively 7.1 and 6.2 mmol h-1 mg-1 protein for aspartic acid and 45 and 9.3 mmol h-1 mg-1 protein for cysteinesulphinic acid. Both enzymes exhibit maximum activity at pH 8.6. A high specific activity is found in optimal conditions for these two transaminases, the pI values being 9.06 and 5.70 for cysteinesulphinate transaminase A and B respectively. These results have been compared with those already obtained for purified aspartate aminotransferase. Similarities in the pathways of taurine and gamma-aminobutyric acid (GABA) metabolism are discussed.

Aging↗

PubMed1990

Kinetic characterization of GABA-transaminase from cultured neurons and astrocytes.

The enzymatic mechanism and the kinetic parameters of GABA-transaminase extracted from cultured mouse cerebral cortex neurons and astrocytes were studied. Neuronal as well as astrocytic GABA-transaminase obeyed a bi bi ping-pong reaction mechanism. The estimated Km-values for alpha-ketoglutarate and GABA were significantly lower for astroglial GABA-transaminase compared to the neuronal enzyme suggesting a possible existence of cell specific isozymes of GABA-transaminase. The observed enzymatic mechanism and the magnitude of the estimated kinetic parameters imply that GABA-transaminase synthesized in the two types of cultured neural cells is mechanistically and kinetically equivalent to the enzyme synthesized in the brain in vivo.

4-Aminobutyrate Transaminase↗

PubMed2004

[Dysferlinopathy as an extrahepatic cause for the elevation of serum transaminases].

BACKGROUND AND PURPOSE: The aim of the present report is to emphasize that the source of elevated transaminase levels, although usually indicative of hepatocellular damage, can also be of extrahepatic origin. CASE REPORT: A 42-year-old female presented with a moderate persistent elevation of the transaminases glutamic-oxaloacetic transaminase (GOT; synonym: aspartate aminotransferase [AST]) and glutamic-pyruvic transaminase (GPT; synonym: alanine aminotransferase [ALT]) in blood without any apparent clinical symptoms of liver affection. In the course of further diagnostics for clarification of a suspected liver disease, a markedly elevated activity of creatine kinase was found which, in concert with results from myography, magnetic resonance imaging (MRI) and analysis of muscle biopsies, suggested the tentative diagnosis of a distal myopathy type Miyoshi. The diagnosis was confirmed by identification of the underlying mutation in the dysferlin gene. The course of the disease has been slowly but steadily progressive; there is no therapeutic option at present. The relevance of molecular genetic analyses in the diagnostic procedure for distal myopathies, in particular dysferlinopathy, is discussed and the characteristics of this disease are summarized. CONCLUSION: In the case of persistent elevations of the serum transaminases GOT and GPT without liver disorder, a myopathy has to be taken into account as a potential extrahepatic source. In order to avoid needless nondirected expensive investigations and to prevent a delay in diagnostics, activity of serum creatine kinase should be determined which is moderately to strongly elevated in the case of myopathies. If, in particular, a dysferlinopathy is supposed, the underlying mutation should be identified to confirm the diagnosis and as a basis for current and future therapeutic interventions

Adult↗

PubMed1987

Studies on the mechanism of acetaldehyde-mediated inhibition of rat liver transaminases.

Incubation of mitochondria-depleted rat liver homogenates with 5 mmol/l acetaldehyde at 37 degrees C for 1 h inhibited both aspartate and alanine aminotransferases by 30%. Inhibition was prevented by decreasing temperature to 4 degrees C or by preincubating homogenates with cyanate but was unaffected by cyanamide and methylpyrazole which block acetaldehyde oxidation and reduction respectively. Cyanate-sensitive acetaldehyde-mediated inhibition of purified porcine heart transaminases was also demonstrated in the presence of rat liver homogenate but not in Tris/sucrose medium. Moreover, porcine transaminases were inhibited by trichloroacetic acid extracts of rat liver homogenates previously incubated with acetaldehyde but not by extracts of homogenates incubated with both acetaldehyde and cyanate. These findings suggest that acetaldehyde-mediated transaminase inhibition requires further non-oxidative metabolism of acetaldehyde. Since transaminase activities were not restored by addition of pyridoxal 5'-phosphate to the assay systems, acetaldehyde-induced transaminase inhibition does not appear to be mediated by displacement or depletion of this B6 coenzyme.

Acetaldehyde↗

PubMed2006

Activities of membrane bound phosphatases, transaminases and mitochondrial enzymes in white spot syndrome virus infected tissues of Fenneropenaeus indicus.

Disease caused by viruses, especially white spot syndrome virus (WSSV), present the greatest challenge to shrimp aquaculture worldwide. Massive tissue disintegration occurs in WSSV-infected ectodermal and mesodermal tissues of penaeid shrimp. The activities of membrane bound phosphatases (Na(+)K(+)ATPase, Ca(2+)ATPase, Mg(2+)ATPase and Total ATPase), transaminases (alanine transaminase (ALT) and aspartate transaminase (AST)) and mitochondrial enzymes (isocitrate dehydrogenase (ICDH), succinate dehydrogenase (SDH), malate dehydrogenase (MDH), alpha-ketoglutarate dehydrogenase (KGDH), NADH dehydrogenase, cytochrome C oxidase) in WSSV-infected tissues (hemolymph, hepatopancreas, gills and muscle) of Fenneropenaeus indicus were determined at intervals after WSSV infection (0, 24, 48, 72 and after 72 h (moribund)). The activities of phosphatases, transaminases and mitochondrial enzymes in healthy as compared with WSSV-infected hemolymph, hepatopancreas, gills and muscle showed marked divergence throughout the course of infection. WSSV infected hemolymph, hepatopancreas, gills and muscle exhibited significantly reduced activity of membrane bound phosphatases compared with the uninfected animals. Inactivation of these enzymes may occur due to increased production of free radicals, that cause conformational change by oxidation of 'SH' groups present at the active site. Significantly marked elevation in the activities of transaminases (ALT and AST) was observed in WSSV-infected hemolymph, hepatopancreas, gills and muscle compared to the uninfected tissues. This may be due to leakage of these enzymes from the damaged tissues. The activities of mitochondrial enzymes in WSSV-infected tissues were significantly decreased compared to the activities in uninfected animals. WSSV-infected animals showed reduced feeding that may have led to decreased oxidation of glucose via the TCA cycle. Excessive production of free radicals in WSSV-infected animals may have affected aerobic oxidation leading to lower production of ATP. It is concluded that membrane dynamics play a major role in the pathogenesis of WSSV infection.

Animals↗