Dysmorphic features in a newborn with neurological, liver and kidney involvement by defective peroxisomal biogenesis. case report

ABSTRACT Introduction: Inborn errors of metabolism have significant morbidity and mortality rates in the neonatal period. One of these disorders is defective peroxisomal biogenesis, which causes complex and severe clinical pictures because peroxisomes are present in all nucleated cells of mammals. Case presentation: This is the case of a newborn with dysmorphic features who had seizures at birth and presented with neurological, liver, kidney and heart involvement during her 20 days of life. Necropsy confirmed liver and kidney involvement, which, together with family history of death of a sibling and a cousin, led to suspect a peroxisomal disease that was confirmed by the biochemical alterations observed. Discussion: Dysmorphism and seizures at birth may be an expression of a metabolic disease. The findings of the physical examination and the demonstration of liver, kidney and heart involvement are consistent with the initial description of Zellweger syndrome; the biochemical alterations are conclusive. Conclusions: It is necessary to define if dysmorphism is an isolated finding or if there is involvement of other organ(s) or system(s) to establish a suitable diagnosis of peroxisome biogenesis. Inborn errors of metabolism should be included in the diagnosis of dysmorphic newborns when several organs are involved, since their identification enables genetic counseling.

RESUMEN Introducción. Los errores innatos del metabolismo pueden ocasionar altas tasa de morbimortalidad en el período neonatal. Dentro de estos trastornos se encuentran los desórdenes en la biogénesis del peroxisoma, que originan cuadros clínicos complejos y graves debido a que los peroxisomas están presentes en todas las células nucleadas de los mamíferos. Presentación del caso. Paciente dismórfica recién nacida quien presentó convulsiones al nacer y desarrolló compromiso neurológico, hepático, renal y cardíaco durante sus 20 días de vida; en la necropsia se confirmó compromiso hepático y renal, por lo que se sospechó de una enfermedad peroxisomal. Las alteraciones bioquímicas reportadas en el presente caso fueron compatibles con un trastorno en la biogénesis de los peroxisomas. Como antecedente se registró la muerte neonatal de un hermano y un primo. Discusión. La presencia de dismorfismo y convulsiones al nacer puede indicar la presencia de una enfermedad metabólica. En la paciente reportada, los hallazgos del examen físico y la demostración del compromiso hepático, renal y cardíaco se ajustan a la descripción inicial del síndrome de Zellweger; por su parte, las alteraciones bioquímicas son concluyentes de un trastorno en la biogénesis de los peroxisomas. Conclusiones. Es necesario definir si el dismorfismo es un hallazgo aislado y si existe afectación de otros órganos o sistemas para establecer un posible diagnóstico de biogénesis de los peroxisomas. Asimismo, los errores innatos del metabolismo deben incluirse en el diagnóstico de los recién nacidos dismórficos cuando hay compromiso de varios órganos, pues su identificación posibilita la asesoría genética.

Laboratory Diagnosis of Peroxisomal Disorders in the -Omics Era and the Continued Importance of Biomarkers and Biochemical Studies

Abstract The clinical as well as biochemical and genetic spectrum of peroxisomal diseases has markedly increased over the last few years, thanks to the revolutionary advances in the field of genome analysis and several -omics technologies. This has led to the recognition of novel disease phenotypes linked to mutations in previously identified peroxisomal genes as well as several hitherto unidentified peroxisomal disorders. Correct interpretation of the wealth of data especially coming from genome analysis requires functional studies at the level of metabolites (peroxisomal metabolite biomarkers), enzymes, and the metabolic pathway(s) involved. This strategy is not only required to identify the true defect in each individual patient but also to determine the extent of the deficiency as described in detail in this article.

Structural and functional roles of ether lipids

Ether lipids, such as plasmalogens, are peroxisome-derived glycerophospholipids in which the hydrocarbon chain at the sn-1 position of the glycerol backbone is attached by an ether bond, as opposed to an ester bond in the more common diacyl phospholipids. This seemingly simple biochemical change has profound structural and functional implications. Notably, the tendency of ether lipids to form non-lamellar inverted hexagonal structures in model membranes suggests that they have a role in facilitating membrane fusion processes. Ether lipids are also important for the organization and stability of lipid raft microdomains, cholesterol-rich membrane regions involved in cellular signaling. In addition to their structural roles, a subset of ether lipids are thought to function as endogenous antioxidants, and emerging studies suggest that they are involved in cell differentiation and signaling pathways. Here, we review the biology of ether lipids and their potential significance in human disorders, including neurological diseases, cancer, and metabolic disorders.

Effect of ctpxa1 gene deletion in Candida tropicalis on long chain dicarboxylic acid accumulation / 生物工程学报

Candida tropicalis uses alkanes and fatty acids to produce long chain dicarboxylic acids. However, the yield can be affected by β-oxidation in peroxisomes. Pxa1p was a membrane protein of Saccharomyces cerevisiae peroxisomes. Pxa1p and Pxa2p form a dimer that is involved in transporting of long chain fatty acids into peroxisomes, but the similar transporting system of Candida tropicalis has not yet been reported. In this study, a ctpxa1 gene deletion strain named C. tropicalis 1798-pxa1 was constructed by homologous single exchange method using PCR fragment. The expression of ctpxa1 gene in C. tropicalis 1798, C. tropicalis 1798-pxa1 was detected by semi-quantitative RT-PCR, and the ratio of gray value was 2.03, implying that the expression of ctpxa1 in C. tropicalis 1798-pxa1 was weakened. After 144 h fermentation, the dodecanedioic acid production of C. tropicalis 1798-pxa1 was increased 94.3% than the former strain, the maximum yield was 10.3 g/L.

Correlation of peroxisome pathway reactive oxygen species oxidative stress gene and its correlation with the antitumor sensitivity of artesunate against pancreatic cancer / 国际肿瘤学杂志

Objective To explore the screening of peroxisome pathway reactive oxygen species (ROS) oxidative stress gene and its correlation with the antitumor sensitivity of artesunate against pancreatic cancer. Methods Based on microarray mRNA expressions of 55 tumor cell lines in the National Cancer Institute common database,peroxisome pathway-related key genes which were significant correlation with half-inhibitory concentration (IC50 )values of artesunate antitumor activity against human pancreatic cancer were selected by Kendall test.The candidate genes associated with artesunate sensitivity were identified and their mRNA expressions in pancreatic cancer cells were tested using fluorescent quantitative PCR.The contents of peroxi-dase in pancreatic cancer cells were detected through the DAB staining.Results Thirteen key genes mRNA expressions in peroxidase pathways were significantly correlated with IC50 values for artesunate antitumor activi-ty.Compared with normal liver cells HL-7702 (1.00),CRAT (2.89 ±0.06),PEX11B (1.90 ±0.07)and PEX16 (1.35 ±0.07)mRNA expression levels were significantly increased in pancreatic cancer Panc-1 cells which sensitive to artesunate (t =33.00,P (1.43 ±0.03),SOD1 (2.07 ±0.04)and SOD2 (1.15 ±0.01)mRNA expression levels were also signifi-cantly increased in Panc-1 cells which sensitive to artesunate (t =11.71,P <0.01;t =35.85,P <0.01;t =13.22,P <0.01).However,PEX12 (0.51 ±0.02),CAT (0.47 ±0.02),PRDX1 (0.43 ±0.01),and SOD1 (0.44 ±0.01)mRNA expression levels in pancreatic cancer BXPC-3 cells which resistant to artesunate were significantly lower than that of HL-7702 cells (t =37.53,P <0.01;t =16.52,P <0.01;t =84.20, P <0.01;t =48.24,P <0.01).DAB staining showed that the positive expression rate of peroxisomal content was apparently higher in Panc-1 cells (61.5%)than that of HL-7702 cells (43.8%),with a significant difference (χ2 =16.11,P <0.01).Conclusion Peroxisome and its related ROS antioxidant enzymes CAT, PRDX1,SOD gene expression may be the important factors that affect artesunate antitumor activity against human pancreatic cancer.

Statins Increase Mitochondrial and Peroxisomal Fatty Acid Oxidation in the Liver and Prevent Non-Alcoholic Steatohepatitis in Mice

BACKGROUND: Non-alcoholic fatty liver disease is the most common form of chronic liver disease in industrialized countries. Recent studies have highlighted the association between peroxisomal dysfunction and hepatic steatosis. Peroxisomes are intracellular organelles that contribute to several crucial metabolic processes, such as facilitation of mitochondrial fatty acid oxidation (FAO) and removal of reactive oxygen species through catalase or plasmalogen synthesis. Statins are known to prevent hepatic steatosis and non-alcoholic steatohepatitis (NASH), but underlying mechanisms of this prevention are largely unknown. METHODS: Seven-week-old C57BL/6J mice were given normal chow or a methionine- and choline-deficient diet (MCDD) with or without various statins, fluvastatin, pravastatin, simvastatin, atorvastatin, and rosuvastatin (15 mg/kg/day), for 6 weeks. Histological lesions were analyzed by grading and staging systems of NASH. We also measured mitochondrial and peroxisomal FAO in the liver. RESULTS: Statin treatment prevented the development of MCDD-induced NASH. Both steatosis and inflammation or fibrosis grades were significantly improved by statins compared with MCDD-fed mice. Gene expression levels of peroxisomal proliferator-activated receptor α (PPARα) were decreased by MCDD and recovered by statin treatment. MCDD-induced suppression of mitochondrial and peroxisomal FAO was restored by statins. Each statin's effect on increasing FAO and improving NASH was independent on its effect of decreasing cholesterol levels. CONCLUSION: Statins prevented NASH and increased mitochondrial and peroxisomal FAO via induction of PPARα. The ability to increase hepatic FAO is likely the major determinant of NASH prevention by statins. Improvement of peroxisomal function by statins may contribute to the prevention of NASH.

Impact of D-bifunctional Protein Deficiency on Telomere Length and Gene Expression in a Child.

Aim: To explore, in one patient, the possibility that D-bifunctional protein (D-BP) deficiency affects telomere length, and to determine the profile of genetic expression. Presentation of Case: Due to the symptoms of a newborn and his family background, a peroxisomal panel was performed. There were high levels of very long chain fatty acids and abnormal peroxisomes. At 8 months the patient exhibited other complications, including progressive multi systemic deterioration, and at 15 months died of pneumonia. Discussion: Analysis of the patient’s fibroblasts provided evidence of a defect in the peroxisomes and in the oxidation of fatty acids, leading to a diagnosis of D-BP deficiency. Significant alterations were found in the genetic expression profile, with the greatest number of affected genes involved in neuronal functions, two implicated in peroxisomal biogenesis, and some others related to telomere protection and DNA repair. The child had a mixture of very short and normal length telomeres, a condition commonly observed in the elderly and in individuals with chronic degenerative diseases. Conclusion: The abnormal function of peroxisomes and altered gene expression found in the patient under study could explain the affected telomere length. Further studies are needed to explore this possibility.

Propriedades antiaterogênicas de novas tiazolidino-2, 4-dionas / Antiatherogenic properties of new thiazolidin-2, 4-diones

Tiazolidinadionas (TZDs) são agentes sensibilizadores de insulina que agem por ligação ao receptor gama ativado por proliferador de peroxissomos (PPARγ). Elas têm apresentado efeitos cardioprotetores em humanos e propriedades anti-aterogênicas em modelos animais. Estudos in vitro têm sugerido que esses efeitos anti-aterogênicos da ativação de PPARγ ocorrem por inibição da expressão de genes pro-inflamatórios e por aumentar o efluxo de colesterol via ativação dos receptores LXR-ABCA1. Entretanto, vários efeitos colaterais são associados ao tratamento com as TZDs, tornando necessária a pesquisa por novos compostos desta classe. Neste estudo, 14 novas tiazolidina-2,4- dionas, que são TZDs modificadas por bioisosterismo, foram avaliadas quanto à expressão de fatores aterogênicos e inflamatórios em linhagens de macrófagos J774 e RAW 264.7 e em camundongos com deleção genética para o receptor de LDL (LDLr-/-). Após a avaliação da citotoxicidade em macrófagos, foram eleitas cinco TZDs, denominadas de GQ-11, GQ-97, GQ-177, GQ-145 e LYSO-7. Três destas TZDs (GQ- 145, GQ-177 e LYSO-7) aumentaram significativamente a expressão de RNAm dos fatores de transcrição PPARγ1, PPARγ2 e do receptor CD36, assim como também aumentaram a expressão gênica de ABCA1 em 2.9, 3.5 e 6.7 vezes, respectivamente. Em adição, estas TZDs diminuíram a expressão gênica de iNOS, COX2, VCAM e IL-6 associado a redução na produção de nitritos, mas apenas a LYSO-7 reduziu significativamente a expressão desses genes quando comparada à rosiglitazona (RSG), além de diminuir a expressão da proteína-1 quimiotática para monócitos (MCP-1). No estudo experimental, os camundongos LDLr-/- machos foram alimentados com dieta hipercolesterolêmica por 16 semanas e quatro semanas antes da eutanásia receberam os derivados tiazolidínicos (20 mg/kg/dia) por gavagem. GQ-177 inibiu a progressão da placa aterosclerótica associada à aumento nas concentrações plasmáticas de HDL-C, com elevação na expressão de ABCA1, e redução da via inflamatória CD40-CD40L. LYSO-7 também mostrou inibição da aterogênese associada à redução das concentrações plasmáticas de colesterol total e triacilgliceróis, com diminuição na interação entre CD40-CD40L e expressão de citocinas inflamatórias. A GQ-145 não alterou os níveis plasmáticos dos lipídeos, mas aumentou a expressão de todos os genes pró-aterogênicos e pró-inflamatórios. Adicionalmente, as vias de ativação destas novas TZDs também foram estudadas por ensaio de luciferase, como gene repórter. A GQ-177 induziu ativação de PPARγ e ligação ao seu domínio, enquanto a LYSO-7 estimulou ativação de PPARα e PPARδ. Portanto, conclui-se que as novas TZDs, especialmente a GQ-177 e a LYSO-7, podem apresentar propriedades ateroprotetoras associadas ao transporte reverso de colesterol e aos efeitos antiinflamatórios, e poderiam ser uma alternativa promissora para o tratamento da aterosclerose. Porém, estudos complementares são requeridos para caracterizar as vias de sinalização intracelular, visto que as duas demonstraram ativar diferentes isotipos do fator de transcrição PPAR

Thiazolidinediones (TZDs) are insulin-sensitizing agents that act by binding to peroxisome proliferator-activated receptor-γ (PPARγ). They have been demonstrated to possess cardioprotective effects in humans and antiatherogenic properties in animal models. In vitro studies have also suggested that these antiatherogenic effects of PPARγ activation occur by inhibiting the inflammatory gene expression and by increasing cholesterol efflux via LXR-ABCA1 activation. However, several side effects are associated with TZDs treatment making necessary the search for new compounds. In this study, 14 new thiazolidine-2,4-diones, modified TZDs by bioisosterism, were tested for aterogenic and inflammtary factors in RAW 264.7 macrophages and in low-density lipoprotein receptor-deficient mice. After the citotoxicity evaluation in RAW 264.7 macrophages the TZDs named GQ-11, GQ-97, GQ-177, GQ-145 e LYSO-7 were selected for this study. Three of these TZDs (GQ-177, GQ-145 and LYSO-7) significantly increased the expression of PPARγ1, PPARγ2 and CD36 mRNA, and enhanced the expression of ABCA1 mRNA in 2.9, 3.5 and 6.7 fold, respectively. Moreover, they also significantly decreased the expression of iNOS, COX2, VCAM and IL-6 mRNA in relation to control, and these results are associated to reduction on nitrits concentration. In addition, LYSO-7 significantly reduced the expression of these genes when compared to rosiglitazone, and decreased expression of MCP1 mRNA. In the experimental study, male LDLr-/- mice were fed an atherogenic diet containing 0.5% cholesterol for 16 weeks, and 4 weeks before euthanasia they received TZDs (20mg/kg/ per day) by gavage. GQ-177 treatment inhibited progression of atherosclerotic plaque associated to increased plasma concentrations of HDL-C, with enhance of ABCA1 expression and reduction on CD40-CD40L interaction. LYSO-7 treatment also showed inhibition of the atherogenesis associated to decreased plasma concentrations of total cholesterol and TAG, with reduction on CD40-CD40L pathway and inflammatory cytokines expression.GQ-145 did not alter the lipid plasma levels and increased the expression of all pro-atherogenic and pro-inflammatory genes. Furthermore, the activation of PPARs has also been studied, by luciferase assay as reporter gene. GQ-177 induced activation of PPARγ, whereas LYSO-7 stimulated activation of PPARα and PPARß/δ. Altogether, our data suggest that the new TZDs derivatives, specially GQ- 177 and LYSO-7, may have atheroprotective properties associated with the reverse cholesterol transport and anti-inflammatory effects, and could be a promising alternative for the treatment of atherosclerosis. However, further studies are warranted in order to characterize the pathways of intracellular signaling since both have demonstrated to activate different isotypes of PPAR

Role of Reactive Oxygen Species in Hypothalamic Regulation of Energy Metabolism

To understand the etiology of metabolic disorders, including obesity and type II diabetes, it is essential to gain better insight into how stored and available energy sources are monitored by the central nervous system. In particular, a comprehension of the fine cellular interplay and intracellular mechanisms that enable appropriate hypothalamic and consequent endocrine and behavioral responses to both circulating hormonal and nutrient signals remains elusive. Recent data, including those from our laboratories, raised the notion that reactive oxygen species (ROS) generation is not merely a by-product of substrate oxidation, but it plays a crucial role in modulating cellular responses involved in the regulation of energy metabolism. These review summarizes the published recent data on the effect of ROS levels in the regulation of neuronal function, including that of hypothalamic melanocortin neurons, pro-opiomelanocortin and neuropeptide Y-/agouti related peptide-neurons, in the modulation of food intake.

Relationship of peroxisome proliferator activated receptor gamma C161T gene polymorphism of elderly patients with metabolic syndrome / 中华老年医学杂志

Objective To investigate the relationship of peroxisome proliferator activated receptor gamma ( PPAR?)C161T gene polymorphism with related diseases of metabolic syndrome. To disscuss the mechanism of the elderly diseases from gene level and the relation between the gene polymorphism and lipid metabolism. Methods Three hundred seventy one non-sibship subjects of Han nationality were investigated in this study, including 69 old healthy subjects, 302 elderly cases diagnosed as metabolic syndrome. PPAR? C161T gene polymorphism was determined by polymerase chain reaction and restriction fragment length polymorphism, and radioimmunoassay was used to detect serum insulin. The insulin resistance was obtained from homeostasis model assessment (HOMA), and blood glucose, blood lipoprotein, height, weight and so on were tested. The frequencies of PPAR? C161T genotypes and the allele were compared with the clinical data. Results (1) In the groups of old normal health and metabolic syndrome, "T" allele frequency was 0.217,0.201, and "C" allele frequency was 0.783, 0.798 . There was no significant difference between the groups. (2)The triglyceride in CC genotypes of the metabolic syndrome was significantly higher than that in "T" allele carriers. Conclusions (1) The distributing trend of PPAR ? C161T gene polymorphism of the Han nationality in Wuhan in the elderly normal healthy group was in accord with that in the group of the elderly metabolic syndrome. (2) PPAR ? C161T substitution can influence metabolic syndrome, especially in liporprotain metabolism. "T" allele is associated with lower level of triglyceride.

Abnormal fat accumulation and changes in peroxisome fatty acids ?-oxidation in liver of obese rats with type 2 diabetes / 解放军医学杂志

Objective To investigate the metabolic changes in free fatty acids in the livers of obese rats with type 2 diabetes.Methods Thirty male SD rats were randomly divided into control group(Con group) and diabetes mellitus group(DM group),with 15 in each group.Rats in Con group and DM group were fed with normal diet and high-fat diet,respectively.Eight weeks later,OGTT and ISI test were performed to identify insulin resistance.Then the insulin-resistant rats received intraperitoneal injection of low-dose streptozocin(STZ) to induce type 2 diabetes.After giving high-fat diet further for six more weeks,8 rats of each group were sacrificed and artery blood and liver sample were obtained for further analysis.The mRNA levels of diacylglycerol O-acyltransferase 1(DGAT1),carnitine palmitoyltransferaseⅠ(CPTⅠ),palmitoyl-CoA oxidase(ACOX1),D-bifunctional protein(DBP) and L-bifunctional protein(LBP),which were involved in fatty acids metabolism,were evaluated by RT-PCR.The protein level of DBP was evaluated by Western blotting Peroxisome fatty acids ?-oxidation was measured by spectrophotometry.Free fatty acids in blood and liver were determined by gas chromatography.Oil red staining was used to determine the fat accumulation in liver.Results The mRNA expressions of DGAT1,CPTⅠ,ACOX1 and LBP increased(P

Role of NF-?B and PPAR-? in the development of Barrett's esophagus and esophageal adenocarcinoma / 解放军医学杂志

Objective To study the role of nuclear factor-?B(NF-?B) and peroxisome proliferation activator receptor-?(PPAR-?) in the development of Barrett's esophagus(BE) and esophagus adenocarcinoma(EA).Methods Fifty BE patients including 25 EA patients admitted in Fuzhou General Hospital of Nanjing Command from Jul.2005 to Jul.2006 were involved in the present study.The expressions of NF-?B and PPAR-? in squamous epithelial cells of normal esophagus,BE and EA were investigated with immunohistochemical staining.The correlation between the expression of both NF-?B and PPAR-? and their clinicopathological features were analyzed.Results Positive staining of NF-?B was situated in cytoplasm,and that of PPAR-? in nuclei.No expression of NF-?B and PPAR-? was found in normal esophageal squamous epithelium,while they expressed in a medium extent in BE(positive staining in cytoplasm of goblet cells and surface glandular epithelium),and extensively expressed in EA.There existed significant difference in expression of NF-?B and PPAR-? in EA compared with those in BE and normal esophageal squamous epithelium(P

Effect of telmisartan on left ventricular hypertrophy in elderly patients with diabetes mellitus and essential hypertension / 中华老年医学杂志

Objective To explore the effect of angiotensin Ⅱ antagonist on left ventricular hypertrophy(LVH) and insulin resistance in elderly patients with diabetes mellitus and hypertension. Methods One hundred and twenty elderly patients with diabetes mellitus and essential hypertension with LVH by echocardiography entered the study. Patients were randomized into the telmisartan (80～160 mg/d) group or perindopril (4～8 mg /d) group. After treatment of telmisartan or perindopril,patients were followed-up for 8 months.Plasma sample was collected from each patient before and after treatment of telmisartan or perindopril,respectively.Then plasma levels of cholesterol,fasting plasma glucose(FPG), insulin and Homeostasis Model Assessment Insulin Resistance (HOMA-IR) were investigated.The echocardiography before and after 8 months of treatment with telmisartan or perindopril were also examined. Results Data were analyzed and showed that: (1)After 8 months of treatment with telmisartan or perindopril, blood pressure was reduced from 159/101 to 142/89 mm Hg(P

Protective effect of rosiglitazone on cyclosporine A-induced nephrotoxicity in rat NRK cells / 中华肾脏病杂志

Objective To investigate the protective effects of rosiglitazone (RSG) on normal rat kidney cells (NRK) damaged by cyclosporine A(CsA). Methods The NRK cells were cultured with CsA or with CsA plus rosiglitazone. The cellular proliferation was determined by MTT colorimetry. The mRNA expression of TGF-?1 and PPAR? was detected by RT-RCR. Protein levels of PPAR?, p-ERK,FN and AT1R were examined by Western blotting. The level of TGF-?1 in the supernatants was measured by enzyme-linked immunosorbant assay (ELISA). Results CsA inhibited the proliferation of NRK cells in dose and time dependent manner (P

Analysis to the relationship between peroxisomes and Salmonella typhimurium in macrophages / 解放军医学杂志

Objective To understand the role of peroxisomes on the intracellular survival of Salmonella typhimurium in macrophages. Methods Vesicles from infected or uninfected RAW264.7 macrophage-like cells were isolated by stepwise centrifugation after cells were broken by nitrogen cavitation and purified with magnetic beads containing polyclonal antibodies to TassC (Target for Salmonella secreted protein SpiC). Western-blot was used to detect the characters of the binding vesicles. Three-dimensional (xyz) fluorescence microscopy was used to determine the recruitment of peroxisomes tagged with pDsRed2-Perxi to the SCV after infection of RAW264.7 cells with Salmonella typhimurium mutant strains spiC:kan producing GFP. Volocity software was employed for image analysis. Overlap of individual fluorescence pixels from separated channels for each optical plane was determined with the Volocity 4.1 colocalization module. Results It was shown by western-blot that the anti-TassC magnetic beads could bind TassC and peroxisomal marker catalase in infected or uninfected RAW264.7 cells. Inducible nitric oxide synthase (iNOS) could be detected in infected samples, but couldn’t in uninfected samples. Lysosome associated membrane protein (LAMP1), one of the lysosome markers, and a bacterium marker RecA could not be detected from the elution of anti-TassC magnetic beads. It was determined by a fluorescence microscopy that the recruitment or overlapping of peroxisomes tagged with pDsRed2-Perxi to the Salmonella-containing vacuoles after infection of RAW264.7 cells with Salmonella mutant strains producing GFP. Calculation by Volocity 4.1 showed that peroxisome abundance increased by 1.2- or 1.3-fold, respectively, at 1h and 24h time point of infection in the infected macrophages than in uninfected cells while the bacteria abundance decreased with the infection time. Conclusion It is suggested that TassC is localized with peroxisomes, but not with lysosomes. Inducible nitric oxide synthase might be localized to peroxisomes and recruited to the SCV during infection with Salmonella mutant strains for killing the bacterium.