28 research outputs found
Rise in 2017-2018 measles morbidity in Serbia and northwest Russia
In 2017, the WHO registered 23,927 measles cases in 44 out of 53 countries in the European region. In 2018, measles incidence rate increased up to 82,599 cases registered in 48 countries of the region, with a large number of measles-associated deaths. Overall, 72 measles fatalities were registered in 10 European countries, including Serbia (15 cases). Aim of the study: to characterize 2017-2018 epidemiological upsurge of measles incidence rate observed in the Republic of Serbia (RS) and the Northwestern Federal District (NWFD) of the Russian Federation. Materials and methods. During the 2017-2018 season, 944 serum samples were collected from patients with measles, rubella, or exanthematous diseases in the NWFD and tested in the Laboratory of Virology at the St. Petersburg Regional Centre for Measles Surveillance (SPbRC). In 2017-2018, 2,946 serum samples from the Republic of Serbia were analyzed in the SPbRC by using ELISA with IgM measles test system (Vector-Best, Russia; or Siemens, Germany). Urine and swab samples were examined by RT-PCR and used for isolation and genotyping of measles viruses. Results. From 2017 to 2018, 5,798 measles cases were registered in the RS, among which 2,946 were laboratory-confirmed (serological testing and/or PCR). Unvaccinated subjects or those with unknown vaccination status accounted for majority of the cases. Children under 5 years of age and adults aged 30 years and over dominated among measles patients. During this season, 15 deaths were reported. Several genotypes of measles virus circulated in the RS, e.g. B3 Dublin, D8 Gir Somnath, and D8 Herborn. In 2018, 109 measles cases were recorded in the NWFD, 5 of which were imported from abroad. Among patients, adults comprised 64.2%, wherein 74.3% were covered by unvaccinated subjects or those with unknown vaccination status. Rise in measles incidence rate linked to multiple importations of various measles virus genotypes: B3 Kabul; B3 Dublin; D8 Frankfurt; D8 Cambridge; and D8 Gir Somnath
ΠΠ°ΡΠ°ΠΎΠΊΡΠΎΠ½Π°Π·Π°: ΡΠ½ΠΈΠ²Π΅ΡΡΠ°Π»ΡΠ½ΡΠΉ ΡΠ°ΠΊΡΠΎΡ Π°Π½ΡΠΈΠΎΠΊΡΠΈΠ΄Π°Π½ΡΠ½ΠΎΠΉ Π·Π°ΡΠΈΡΡ ΠΎΡΠ³Π°Π½ΠΈΠ·ΠΌΠ° ΡΠ΅Π»ΠΎΠ²Π΅ΠΊΠ°
The paraoxonase (PON) gene family includes three members: PON1, PON2, and PON3 aligned in tandem on chromosome 7 in humans. All PON proteins share considerable structural homology and have the capacity to protect cells from oxidative stress; therefore, they have been implicated in the pathogenesis of several inflammatory diseases, particularly atherosclerosis. Increased production of reactive oxygen species as a result of decreased activities of mitochondrial electron transport chain complexes plays a role in the development of many inflammatory diseases, including atherosclerosis. PON1 and PON3 proteins can be detected in plasma and reside in the high-density lipoprotein fraction and protect against oxidative stress by hydrolyzing certain oxidized lipids in lipoproteins, macrophages, and atherosclerotic lesions. Paraoxonase 2 (PON2) possesses antiatherogenic properties and is associated with lower ROS levels. PON2 is involved in the antioxidative and anti-inflammatory response in intestinal epithelial cells. In contrast to PON1 and PON3, PON2 is cell-associated and is not found in plasma. It is widely expressed in a variety of tissues, including the kidney, and protects against cellular oxidative stress. Overexpression of PON2 reduces oxidative status, prevents apoptosis in vascular endothelial cells, and inhibits cell-mediated low density lipoprotein oxidation. PON2 also inhibits the development of atherosclerosis, via mechanisms involving the reduction of oxidative stress. In this review we explore the physiological roles of PON in disease development and modulation of PONs by infective (bacterial, viral) agents.ΠΠ°ΡΠ°ΠΎΠΊΡΠΎΠ½Π°Π·Ρ β ΡΡΠΎ ΡΠ΅ΠΌΠ΅ΠΉΡΡΠ²ΠΎ ΡΠ΅ΡΠΌΠ΅Π½ΡΠΎΠ², ΠΏΡΠ΅Π΄ΡΡΠ°Π²Π»Π΅Π½Π½ΠΎΠ΅ PON1, PON2 ΠΈ PON3, ΠΊΠΎΡΠΎΡΡΠ΅ ΠΎΠ±Π»Π°Π΄Π°ΡΡ ΡΠΈΡΠΎΠΊΠΎΠΉ ΡΠΏΠ΅ΡΠΈΡΠΈΡΠ½ΠΎΡΡΡΡ ΠΈ ΠΊΠ°ΡΠ°Π»ΠΈΡΠΈΡΠ΅ΡΠΊΠΎΠΉ ΡΠ½ΠΈΠ²Π΅ΡΡΠ°Π»ΡΠ½ΠΎΡΡΡΡ. PON1 ΠΈ PON3 ΡΠΈΡΠΊΡΠ»ΠΈΡΡΡΡ Π² ΠΏΠ»Π°Π·ΠΌΠ΅ Π² ΡΠΎΡΡΠΎΡΠ½ΠΈΠΈ, ΡΠ²ΡΠ·Π°Π½Π½ΠΎΠΌ Ρ Π»ΠΈΠΏΠΎΠΏΡΠΎΡΠ΅ΠΈΠ½Π°ΠΌΠΈ Π²ΡΡΠΎΠΊΠΎΠΉ ΠΏΠ»ΠΎΡΠ½ΠΎΡΡΠΈ, ΠΏΡΠ΅Π΄ΠΎΡΠ²ΡΠ°ΡΠ°ΡΡ ΠΎΠΊΠΈΡΠ»Π΅Π½ΠΈΠ΅ Π»ΠΈΠΏΡΠΎΠΏΡΠΎΡΠ΅ΠΈΠ½ΠΎΠ², ΡΠΌΠ΅Π½ΡΡΠ°ΡΡ ΠΎΠ±ΡΠ°Π·ΠΎΠ²Π°Π½ΠΈΠ΅ Π»ΠΈΠΏΠΈΠ΄Π½ΡΡ
ΠΏΠ΅ΡΠΎΠΊΡΠΈΠ΄ΠΎΠ² ΠΈ ΡΠ½ΠΈΠΆΠ°ΡΡ ΡΠΈΡΠΊ ΡΠ°Π·Π²ΠΈΡΠΈΡ Π°ΡΠ΅ΡΠΎΡΠΊΠ»Π΅ΡΠΎΠ·Π°. PON2 ΡΠ²Π»ΡΠ΅ΡΡΡ Π²Π½ΡΡΡΠΈΠΊΠ»Π΅ΡΠΎΡΠ½ΡΠΌ ΡΠ΅ΡΠΌΠ΅Π½ΡΠΎΠΌ ΠΈ Π½Π΅ ΠΎΠ±Π½Π°ΡΡΠΆΠΈΠ²Π°Π΅ΡΡΡ Π² ΠΏΠ»Π°Π·ΠΌΠ΅. Β PON2 ΠΎΠ±Π½Π°ΡΡΠΆΠ΅Π½Π° Π²ΠΎ ΠΌΠ½ΠΎΠ³ΠΈΡ
ΡΠΊΠ°Π½ΡΡ
ΠΎΡΠ³Π°Π½ΠΈΠ·ΠΌΠ°, Π²ΠΊΠ»ΡΡΠ°Ρ ΠΏΠ΅ΡΠ΅Π½Ρ, Π»Π΅Π³ΠΊΠΈΠ΅, ΡΡΠ°Ρ
Π΅Ρ, ΠΏΠΎΡΠΊΠΈ, ΡΠ΅ΡΠ΄ΡΠ΅, ΠΏΠΎΠ΄ΠΆΠ΅Π»ΡΠ΄ΠΎΡΠ½ΡΡ ΠΆΠ΅Π»Π΅Π·Ρ, ΡΠΎΠ½ΠΊΠΈΠΉ ΠΊΠΈΡΠ΅ΡΠ½ΠΈΠΊ, ΠΌΡΡΡΡ, ΡΠ΅ΠΌΠ΅Π½Π½ΠΈΠΊΠΈ ΠΈ ΡΠ½Π΄ΠΎΡΠ΅Π»ΠΈΠ°Π»ΡΠ½ΡΠ΅ ΠΊΠ»Π΅ΡΠΊΠΈ. PON2 ΡΠ°ΠΊΠΆΠ΅ ΠΏΡΠΈΡΡΡΡΡΠ²ΡΠ΅Ρ Π² Π΄ΠΎΡΠ°ΠΌΠΈΠ½Π΅ΡΠ³ΠΈΡΠ΅ΡΠΊΠΈΡ
ΠΎΠ±Π»Π°ΡΡΡΡ
Π³ΠΎΠ»ΠΎΠ²Π½ΠΎΠ³ΠΎ ΠΌΠΎΠ·Π³Π° ΠΈ Π² Π°ΡΡΡΠΎΡΠΈΡΠ°Ρ
. ΠΠ° ΡΡΠ±ΠΊΠ»Π΅ΡΠΎΡΠ½ΠΎΠΌ ΡΡΠΎΠ²Π½Π΅, PON2 Π»ΠΎΠΊΠ°Π»ΠΈΠ·ΡΠ΅ΡΡΡ Π² ΠΌΠΈΡΠΎΡ
ΠΎΠ½Π΄ΡΠΈΡΡ
, Π³Π΄Π΅ ΠΏΡΠ΅Π΄ΠΎΡΠ²ΡΠ°ΡΠ°Π΅Ρ Π½Π°ΠΊΠΎΠΏΠ»Π΅Π½ΠΈΠ΅ ΡΡΠΈΠ³Π»ΠΈΡΠ΅ΡΠΈΠ΄ΠΎΠ² ΠΈ ΡΠ°Π·Π²ΠΈΡΠΈΠ΅ ΠΎΠΊΠΈΡΠ»ΠΈΡΠ΅Π»ΡΠ½ΠΎΠ³ΠΎ ΡΡΡΠ΅ΡΡΠ°. PON3 - ΠΏΠΎΡΠ»Π΅Π΄Π½ΡΡ ΠΈΠ· ΠΎΡΠΊΡΡΡΡΡ
ΠΏΠ°ΡΠ°ΠΎΠΊΡΠΎΠ½Π°Π· ΠΎΠ±Π»Π°Π΄Π°Π΅Ρ Π±ΠΎΠ»Π΅Π΅ Π²ΡΡΠ°ΠΆΠ΅Π½Π½ΠΎΠΉ Π°Π½ΡΠΈΠΊΡΠΈΠ΄Π°Π½ΡΠ½ΠΎΠΉ Π°ΠΊΡΠΈΠ²Π½ΠΎΡΡΡΡ. PON3 ΠΎΠ±Π½Π°ΡΡΠΆΠ΅Π½Π° Π² ΠΊΠ»Π΅ΡΠΊΠ°Ρ
ΠΊΠΎΠΆΠΈ, ΡΠ»ΡΠ½Π½ΡΡ
ΠΆΠ΅Π»Π΅Π·Π°Ρ
, ΠΆΠ΅Π»Π΅Π·ΠΈΡΡΠΎΠΌ ΡΠΏΠΈΡΠ΅Π»ΠΈΠΈ ΠΆΠ΅Π»ΡΠ΄ΠΊΠ°, ΠΊΠΈΡΠ΅ΡΠ½ΠΈΠΊΠ°, ΡΠ½Π΄ΠΎΠΌΠ΅ΡΡΠΈΠΈ, Π³Π΅ΠΏΠ°ΡΠΎΡΠΈΡΠ°Ρ
,Β ΠΊΠ»Π΅ΡΠΊΠ°Ρ
ΠΏΠΎΠ΄ΠΆΠ΅Π»ΡΠ΄ΠΎΡΠ½ΠΎΠΉ ΠΆΠ΅Π»Π΅Π·Ρ, ΡΠ΅ΡΠ΄ΡΠ΅, ΠΆΠΈΡΠΎΠ²ΠΎΠΉ ΡΠΊΠ°Π½ΠΈ ΠΈ Π² Π»Π΅Π³ΠΎΡΠ½ΠΎΠΌ ΡΠΏΠΈΡΠ΅Π»ΠΈΠΈ. PON3 Π½Π΅Π΄ΠΎΡΡΠ°ΡΠΎΡΠ½ΠΎ ΠΈΠ·ΡΡΠ΅Π½Π°, Π½ΠΎ Π΄ΠΎΠΊΠ°Π·Π°Π½ΠΎ Π΅Π΅ Π°Π½ΡΠΈΠΎΠΊΡΠΈΠ΄Π°Π½ΡΠ½ΠΎΠ΅, ΠΏΡΠΎΡΠΈΠ²ΠΎΠ²ΠΎΡΠΏΠ°Π»ΠΈΡΠ΅Π»ΡΠ½ΠΎΠ΅ ΠΈ ΠΏΡΠΎΡΠΈΠ²ΠΎΠΌΠΈΠΊΡΠΎΠ±Π½ΠΎΠ΅ Π΄Π΅ΠΉΡΡΠ²ΠΈΠ΅Β Π·Π° ΡΡΠ΅Ρ Π±Π»ΠΎΠΊΠΈΡΠΎΠ²Π°Π½ΠΈΡ ΠΊΠ²ΠΎΡΡΠΌ-Π·Π°Π²ΠΈΡΠΈΠΌΡΡ
ΡΠΈΡΡΠ΅ΠΌ Π±Π°ΠΊΡΠ΅ΡΠΈΠΉ. ΠΠ·Π±ΡΡΠΎΡΠ½Π°Ρ ΡΠΊΡΠΏΡΠ΅ΡΡΠΈΡ PON3 ΡΠΌΠ΅Π½ΡΡΠ°Π΅Ρ ΠΎΠ±ΡΠ°Π·ΠΎΠ²Π°Π½ΠΈΠ΅ Π°ΡΠ΅ΡΠΎΡΠΊΠ»Π΅ΡΠΎΡΠΈΡΠ΅ΡΠΊΠΈΡ
Π±Π»ΡΡΠ΅ΠΊ ΠΈ ΠΏΡΠ΅ΠΏΡΡΡΡΠ²ΡΠ΅Ρ ΡΠ°Π·Π²ΠΈΡΠΈΡ ΠΎΠΆΠΈΡΠ΅Π½ΠΈΡ, ΠΊΠΎΠ»ΠΈΡΠ΅ΡΡΠ²ΠΎ PON3 ΡΠ²Π΅Π»ΠΈΡΠΈΠ²Π°Π΅ΡΡΡ ΠΏΡΠΈ ΠΎΠ½ΠΊΠΎΠ»ΠΎΠ³ΠΈΡΠ΅ΡΠΊΠΈΡ
Π·Π°Π±ΠΎΠ»Π΅Π²Π°Π½ΠΈΡΡ
, ΠΏΠΎΠ²ΡΡΠ°Ρ ΡΠΎΠΏΡΠΎΡΠΈΠ²Π»Π΅Π½ΠΈΠ΅ ΠΎΠΏΡΡ
ΠΎΠ»Π΅Π²ΡΡ
ΠΊΠ»Π΅ΡΠΎΠΊ ΠΊ ΠΎΠΊΡΠΈΠ΄Π°ΡΠΈΠ²Π½ΠΎΠΌΡ ΡΡΡΠ΅ΡΡΡ ΠΈ Π°ΠΏΠΎΠΏΡΠΎΠ·Ρ.
Π ΠΎΠ±Π·ΠΎΡΠ΅ ΠΏΡΠ΅Π΄ΡΡΠ°Π²Π»Π΅Π½Π° ΠΈΠ½ΡΠΎΡΠΌΠ°ΡΠΈΡ ΠΎ ΡΠΈΠ·ΠΈΠΎΠ»ΠΎΠ³ΠΈΡΠ΅ΡΠΊΠΎΠΉ ΡΠΎΠ΄ΠΈ ΠΏΠ°ΡΠ°ΠΎΠΊΡΠΎΠ½Π°Π·, Π° ΡΠ°ΠΊΠΆΠ΅ ΠΈΡ
ΡΡΠ°ΡΡΠΈΠΈ Π² ΡΠ°Π·Π²ΠΈΡΠΈΠΈ Π·Π°Π±ΠΎΠ»Π΅Π²Π°Π½ΠΈΠΉ, Π°ΡΡΠΎΡΠΈΠΈΡΠΎΠ²Π°Π½Π½ΡΡ
Ρ ΠΎΠΊΠΈΡΠ»ΠΈΡΠ΅Π»ΡΠ½ΡΠΌ ΡΡΡΠ΅ΡΡΠΎΠΌ (Π°ΡΠ΅ΡΠΎΡΠΊΠ»Π΅ΡΠΎΠ·, ΡΠ½Π΄ΠΎΠΌΠ΅ΡΡΠΈΠΎΠ·, Π±ΠΎΠ»Π΅Π·Π½Ρ ΠΠ°ΡΠΊΠΈΠ½ΡΠΎΠ½Π°, ΡΠΈΡΡΠΎΠ· ΠΏΠ΅ΡΠ΅Π½ΠΈ, Π±Π°ΠΊΡΠ΅ΡΠΈΠ°Π»ΡΠ½ΡΠ΅ ΠΈ Π²ΠΈΡΡΡΠ½ΡΠ΅ ΠΈΠ½ΡΠ΅ΠΊΡΠΈΠΈ ΠΈ ΠΎΠΏΡΡ
ΠΎΠ»Π΅Π²ΡΠ΅ ΠΏΡΠΎΡΠ΅ΡΡΡ)
Establishment of murine hybridoma cells producing antibodies against spike protein of sarsβcovβ2
In 2020 the world faced the pandemic of COVIDβ19 severe acute respiratory syndrome caused by a new type of coronavirus named SARSβCoVβ2. To stop the spread of the disease, it is crucial to create molecular tools allowing the investigation, diagnoses and treatment of COVIDβ19. One of such tools are monoclonal antibodies (mAbs). In this study we describe the development of hybridoma cells that can produce mouse mAbs against receptor binding domain of SARSβCoVβ2 spike (S) protein. These mAbs are able to specifically detect native and denatured S proteins in all tested applications, including immunoblotting, enzymeβlinked immunosorbent assay, immunofluorescence staining of cells and immunohistochemical staining of paraffin embedded patientsβ tissue samples. In addition, we showed that the obtained mAbs can efficiently block SARSβ CoVβ2 infection in in vitro experiments. Finally, we determined the amino acid sequence of light and heavy chains of the mAbs. This information will allow the use of corresponding peptides to establish genetically engineered therapeutic antibodies. To date multiple mAbs against SARSβCoVβ 2 proteins have been established, however, bigger sets of various antibodies will allow the detection and neutralization of SARSβCoVβ2, even if the virus acquires novel mutations. Β© 2020, MDPI AG. All rights reserved
Effect of deuterium on the morpho-functional characteristics of normal and cancer cells in vitro
Objective: The aim of our study was to describe effects of different deuterium concentration on morphology and migratory activity of normal stem cells and cancer cell lines in vitro. Materials and methosj51 Water with different deuterium content was used for the culture media preparation: deuterium-depleted water (ddw, D/H = 1 ppm), deutereted (deuterium-rich) water (D/H = 99 abs. At. D%); water with natural deuterium content (MiliQ system) (D/H = 150 ppm) served as control. The cells were cultured in DMEM: F12 supplemented with 10% FBS, 2 mM L-glutamine, and 1 ng/mL FGF-2 in a multi-gas incubator at 5% CO2 and 5% O-2. The morphology of adipose-derived mesenchymal stem cells (ADSCs) was observed after 24 and 72 hours cultivation in experimental media. After incubating for 0, 12, 24, and 48 hours, the gap width of scratch re-population was measured and recorded, and then compared with the initial gap size at 0 hours. Results: High deuterium concentration in culture medium leads to significant morphological changes in normal ADSCs that are associated with cellular stress. Moreover, the migratory activity of ADSCs was inhibited under the deutereted water. At the same time. ddw did not influence morphology or migration of ADSCs. Bothdeutereted water and ddw strongly inhibited migration of cancer cell lines A549 and HT29. Conclusion: Our findings demonstrated that deuterium could act as regulator of biological properties of normal and cancer cells in vitro. However, the mechanisms that underlie the deuterium-mediated effect on different cellular types need to be further investigated
PECULIARITIES OF BREAST FEEDING OF PREMATURE CHILDREN
The article presents main strategies of breast feeding of prematurely born infants support, such as use of Philips AVENT breast pumpfor lactation formation and feeding of the infant with native breast milk.Key words: premature infants, nursing mother, breast feeding support, modern accessories for breast feeding support. (Voprosy sovremennoi pediatrii βΒ Current Pediatrics. 2011; 10 (6): 170β175
Effect of deuterium on the morpho-functional characteristics of normal and cancer cells in vitro
Objective: The aim of our study was to describe effects of different deuterium concentration on morphology and migratory activity of normal stem cells and cancer cell lines in vitro. Materials and methosj51 Water with different deuterium content was used for the culture media preparation: deuterium-depleted water (ddw, D/H = 1 ppm), deutereted (deuterium-rich) water (D/H = 99 abs. At. D%); water with natural deuterium content (MiliQ system) (D/H = 150 ppm) served as control. The cells were cultured in DMEM: F12 supplemented with 10% FBS, 2 mM L-glutamine, and 1 ng/mL FGF-2 in a multi-gas incubator at 5% CO2 and 5% O-2. The morphology of adipose-derived mesenchymal stem cells (ADSCs) was observed after 24 and 72 hours cultivation in experimental media. After incubating for 0, 12, 24, and 48 hours, the gap width of scratch re-population was measured and recorded, and then compared with the initial gap size at 0 hours. Results: High deuterium concentration in culture medium leads to significant morphological changes in normal ADSCs that are associated with cellular stress. Moreover, the migratory activity of ADSCs was inhibited under the deutereted water. At the same time. ddw did not influence morphology or migration of ADSCs. Bothdeutereted water and ddw strongly inhibited migration of cancer cell lines A549 and HT29. Conclusion: Our findings demonstrated that deuterium could act as regulator of biological properties of normal and cancer cells in vitro. However, the mechanisms that underlie the deuterium-mediated effect on different cellular types need to be further investigated
Paraoxonase: The universal factor of antioxidant defense in Human Body
The paraoxonase (PON) gene family includes three members: PON1, PON2, and PON3 aligned in tandem on chromosome 7 in humans. All PON proteins share considerable structural homology and have the capacity to protect cells from oxidative stress; therefore, they have been implicated in the pathogenesis of several inflammatory diseases, particularly atherosclerosis. Increased production of reactive oxygen species as a result of decreased activities of mitochondrial electron transport chain complexes plays a role in the development of many inflammatory diseases, including atherosclerosis. PON1 and PON3 proteins can be detected in plasma and reside in the high-density lipoprotein fraction and protect against oxidative stress by hydrolyzing certain oxidized lipids in lipoproteins, macrophages, and atherosclerotic lesions. Paraoxonase 2 (PON2) possesses antiatherogenic properties and is associated with lower ROS levels. PON2 is involved in the antioxidative and anti-inflammatory response in intestinal epithelial cells. In contrast to PON1 and PON3, PON2 is cell-associated and is not found in plasma. It is widely expressed in a variety of tissues, including the kidney, and protects against cellular oxidative stress. Overexpression of PON2 reduces oxidative status, prevents apoptosis in vascular endothelial cells, and inhibits cell-mediated low density lipoprotein oxidation. PON2 also inhibits the development of atherosclerosis, via mechanisms involving the reduction of oxidative stress. In this review we explore the physiological roles of PON in disease development and modulation of PONs by infective (bacterial, viral) agents
Paraoxonase: The universal factor of antioxidant defense in Human Body
The paraoxonase (PON) gene family includes three members: PON1, PON2, and PON3 aligned in tandem on chromosome 7 in humans. All PON proteins share considerable structural homology and have the capacity to protect cells from oxidative stress; therefore, they have been implicated in the pathogenesis of several inflammatory diseases, particularly atherosclerosis. Increased production of reactive oxygen species as a result of decreased activities of mitochondrial electron transport chain complexes plays a role in the development of many inflammatory diseases, including atherosclerosis. PON1 and PON3 proteins can be detected in plasma and reside in the high-density lipoprotein fraction and protect against oxidative stress by hydrolyzing certain oxidized lipids in lipoproteins, macrophages, and atherosclerotic lesions. Paraoxonase 2 (PON2) possesses antiatherogenic properties and is associated with lower ROS levels. PON2 is involved in the antioxidative and anti-inflammatory response in intestinal epithelial cells. In contrast to PON1 and PON3, PON2 is cell-associated and is not found in plasma. It is widely expressed in a variety of tissues, including the kidney, and protects against cellular oxidative stress. Overexpression of PON2 reduces oxidative status, prevents apoptosis in vascular endothelial cells, and inhibits cell-mediated low density lipoprotein oxidation. PON2 also inhibits the development of atherosclerosis, via mechanisms involving the reduction of oxidative stress. In this review we explore the physiological roles of PON in disease development and modulation of PONs by infective (bacterial, viral) agents
The role of paraoxonases in the pathogenesis of inflammatory and infectious diseases and cancer
The paraoxonase (PON) gene family contains three members: PON1, PON2, and PON3. All the three members of the family possess antioxidant properties and lipo-lactonase activity, and play a role in the pathogenesis of many inflammatory diseases, including atherosclerosis, Alzheimerβs and Parkinsonβs diseases, diabetes mellitus, and cancer. Recent studies have demonstrated that the intracellular paraoxonases PON2 and PON3 associated with mitochondria and mitochondria-associated endoplasmic reticulum membranes regulate mitochondrial superoxide production and prevent apoptosis. As oxidative stress is a result of mitochondrial dysfunction and is involved in the development of inflammatory diseases, including atherosclerosis and cancer, the studies of the enzymes PON2 and PON3 can initiate many epidemiological surveys conducted to search for a relationship between the paraoxonase genes and the development of many inflammatory diseases. Understanding these mechanisms will be able to introduce new treatments for oxidative stress-related diseases. Β© Bionika Media Ltd.. All rights reserved