Biomedical subjects

Rui Curi

Publications and source records attributed to Rui Curi.

At least 73 records · Page 4Linked to original sources

PubMed2003

Genes regulated by arachidonic and oleic acids in Raji cells.

FA are known to modulate immune function in conditions such as arthritis and lupus erythematosus. The effects of arachidonic (AA) and oleic acids (OA) on function and pleiotropic gene expression of Raji cells were investigated. The following parameters were evaluated: cytotoxicity as assessed by loss of membrane integrity and DNA fragmentation; proliferation as measured by [14C]thymidine incorporation; production of interleukin (IL)-10, interferon (INF)-gamma, and tumor necrosis factor (TNF)-alpha; and expression of pleiotropic genes by a macroarray technique (83 genes in total). AA was more toxic to Raji cells than OA. Both FA promoted an increase in Raji cell proliferation at 75 microM, whereas OA at high concentrations (200 microM) decreased proliferation. AA reduced the production of IL-10, TNF-alpha, and INF-gamma. On the other hand, OA provoked an increase of INF-gamma production but did not affect the production of IL-10 and TNF-alpha. The proportions of genes with altered expression were 27% for AA and 35% for OA. The FA affected the expression of genes clustered as: cytokines, signal transduction pathways, transcription factors, cell cycle, defense and repair, apoptosis, DNA synthesis, cell adhesion, cytoskeleton, and hormone receptors. The most remarkable changes were observed in the genes of signal transduction pathways. These results led us to conclude that the effect of these FA on B-lymphocytes includes regulation of gene expression. Thus, diets enriched with fat containing OA or AA may affect B lymphocyte function in vivo.

Arachidonic Acid↗

PubMed2003

Cancer cachexia and tumor growth reduction in Walker 256 tumor-bearing rats supplemented with N-3 polyunsaturated fatty acids for one generation.

In this study we investigated the effect of lifelong supplementation of the diet with coconut oil (CO, rich in saturated fatty acids) or fish oil (FO, rich in n-3 polyunsaturated fatty acids, PUFAs) on tumor growth, animal survival, and metabolic indicators of cachexia in adult rats. Female Wistar rats were supplemented with CO or FO prior to mating and then throughout pregnancy and gestation, and then the male offspring were supplemented from weaning until 90 days of age. Then they were inoculated subcutaneously with Walker 256 tumor cells. Tumor weight at 14 days in control rats (those fed standard chow) was approximately 20 g. These animals displayed cancer cachexia, which was characterized by loss of weight, hypoglycemia, hyperlacticidemia, hypertriacylglycerolemia, and depletion of glycogen stores. Supplementation of the diet with CO did not change these parameters, except that there was a smaller decrease in serum triacylglycerol concentration. Supplementation of the diet with FO significantly decreased tumor growth (by approximately 60%), increased survival (50% at 30 days postinoculation vs. 30% in the controls and 13.5% in the CO group), and prevented the fall in body weight. Furthermore, FO supplementation partly abolished the fall in serum glucose, totally prevented the elevation in serum lactate concentrations, partly prevented the hypertriacylgylcerolemia, and preserved tissue glycogen stores. Lifelong consumption of FO, rich in n-3 PUFAs, protects against tumor growth and cancer cachexia and improves survival.

Analysis of Variance↗

PubMed2003

Improvement of the mitochondrial antioxidant defense status prevents cytokine-induced nuclear factor-kappaB activation in insulin-producing cells.

Proinflammatory cytokines (interleukin-1beta [IL-1beta], tumor necrosis factor-alpha [TNF-alpha], and gamma-interferon [IFN-gamma]) initiate a variety of signal cascades in pancreatic beta-cells that affect the expression level of genes involved in both the destruction and the protection of the beta-cell. The generation of nitric oxide (NO) via the inducible NO synthase (iNOS) and oxygen free radicals play a key role in cytokine-mediated beta-cell destruction. Within these signal cascades, the activation of the transcription factor nuclear factor-kappaB (NF-kappaB) is crucial, and many cytokine-sensitive genes contain binding sites for this transcription factor in their promoter regions. The aim of this study was to characterize the cytokine-mediated activation of NF-kappaB and the subsequent expression of iNOS protein in insulin-producing RINm5F cells with an improved antioxidant defense status by overexpression of the cytoprotective enzymes catalase (Cat), glutathione peroxidase (Gpx), and the cytoplasmic Cu/Zn superoxide dismutase (Cu/ZnSOD). RINm5F cells with diverse mitochondrial antioxidative defense status were generated by stable overexpression of MnSOD constructs in sense (MnSOD sense) and antisense orientation (MnSOD antisense). Cytokine-induced (IL-1beta or cytokine mix consisting of IL-1beta + TNF-alpha + IFN-gamma) activation of NF-kappaB in RINm5F cells was reduced by >80% through overexpression of MnSOD. The activity of the iNOS promoter remained at basal levels in cytokine-stimulated MnSOD sense cells. In contrast, the suppression of MnSOD gene expression in cytokine-stimulated MnSOD antisense cells resulted in a threefold higher activation of NF-kappaB and a twofold higher activation of the iNOS promoter as compared with control cells. The iNOS protein expression was significantly reduced after a 6- and 8-h cytokine incubation of MnSOD sense cells. The low activity level of MnSOD in RINm5F MnSOD antisense cells increased the iNOS protein expression in particular during the early phase of cytokine-mediated toxicity. Cat, Gpx, and the cytoplasmic Cu/ZnSOD did not affect the activation of NF-kappaB and the iNOS promoter. In conclusion, the overexpression of MnSOD, which inactivates specifically mitochondrially derived oxygen free radicals, significantly reduced the activation of NF-kappaB in insulin-producing cells. As a consequence of this protective effect in the early cytokine signaling pathways, the induction of iNOS, an important event in the beta-cell destruction process, was also significantly reduced. The results provide evidence that mitochondrially derived reactive oxygen species (ROS) play a critical role in the activation of the cytokine-sensitive transcription factor NF-kappaB. Overexpression of MnSOD may thus be beneficial for beta-cell survival through suppression of oxygen free radical formation, prevention of NF-kappaB activation, and iNOS expression.

Animals↗

PubMed2003

Pancreatic beta-cells express phagocyte-like NAD(P)H oxidase.

The presence of a phagocyte-like NAD(P)H oxidase in pancreatic beta-cells was investigated. Three NAD(P)H oxidase components were found in pancreatic islets by RT-PCR: gp91(PHOX), p22(PHOX), and p47(PHOX). The components p67(PHOX) and p47(PHOX) were also demonstrated by Western blotting. Through immunohistochemistry, p47(PHOX) was mainly found in the central area of the islet, confirming the expression of this component by insulin-producing cells. Activation of NAD(P)H oxidase complex in the beta-cells was also examined by immunohistochemistry. The pancreatic islets presented slower kinetics of superoxide production than HIT-T15 cells, neutrophils, and macrophages, but they reached 66% that of the neutrophil nitroblue tetrazolium (NBT) reduction after 2 h of incubation. Glucose (5.6 mmol/l) increased NBT reduction by 75% when compared with control. The involvement of protein kinase C (PKC) in the stimulatory effect of glucose was confirmed by incubation of islets with phorbol myristate acetate (a PKC activator) and bysindoylmaleimide (GF109203X) (a PKC-specific inhibitor). Diphenylene iodonium [an NAD(P)H oxidase inhibitor] abolished the increase of NBT reduction induced by glucose, confirming the NAD(P)H oxidase activity in pancreatic islets. Because reactive oxygen species are involved in intracellular signaling, the phagocyte-like NAD(P)H oxidase activation by glucose may play an important role for beta-cell functioning.

Animals↗

PubMed2002

Changes in superoxide dismutase and catalase activities of rat brain regions during early global transient ischemia/reperfusion.

It has been widely recognized that the hippocampus and striatum are clearly more susceptible to oxidative stress than the remaining brain regions. However, the mechanism involved is not known. The activities of the antioxidant enzymes CuZn-superoxide dismutase (SOD), Mn-SOD and catalase were measured in the hippocampus and striatum and the results were compared to cortex and cerebellum (less susceptible to oxidative stress) after 3 h of a global transient ischemia/reperfusion. CuZn-SOD activities were reduced in all brain regions, but mainly in the hippocampus and striatum. Mn-SOD activity was lowered in the striatum, whereas catalase activity was reduced in the hippocampus and striatum. Our findings indicate that in the earlier phase of ischemia/reperfusion the decay in activities of catalase and SOD may be related with the high susceptibility of the hippocampus and striatum to oxidative damage.

Animals↗

PubMed2002

Low proliferation capacity of lymphocytes from alloxan-diabetic rats: involvement of high glucose and tyrosine phosphorylation of Shc and IRS-1.

The proliferation capacity of lymphocytes obtained from mesenteric lymph nodes of control and alloxan-diabetic (40 mg/kg) rats in response to concanavalin A (ConA) and lipopolysaccharide (LPS) stimuli was examined. Proliferation response of lymphocytes from diabetic rats was significantly reduced under Con A (43%) and LPS (46%) stimulation as compared with the control group. Insulin (166 microM) promoted a marked increase of lymphocyte proliferation (7.5-fold) in the control group and this response was much lower (2.6-fold) in lymphocyte from diabetic rats. Cells were also cultured in medium containing glucose at 5, 10 or 20 mM. High glucose concentration (20 mM) caused a marked inhibition of lymphocyte proliferation reaching the values of the diabetic group. In lymphocytes from control rats, the degree of Shc tyrosine phosphorylation was gradually increased, whereas that of cells from diabetic rats was much lower in response to insulin. In lymphocytes obtained from control rats, the tyrosine phosphorylation of IRS-1 was time-dependent on insulin. In cells from diabetic rats, the basal tyrosine phosphorylation of IRS-1 was higher than that of control rats, however, there was no further phosphorylation after insulin addition. We conclude that the response of lymphocyte proliferation from diabetic rats to Con A and LPS stimuli is decreased but insulin was able to promote a significant proliferative effect on these cells. Also, high glycemia in addition to the lack of insulin participates in the reduced proliferation capacity of lymphocytes from diabetic rats.

Alloxan↗

PubMed2002

Evidence that glutamine is involved in neutrophil function.

Phosphate-dependent glutaminase (PDG) activity, a key enzyme of glutamine metabolism, was determined in neutrophils obtained from the intra-peritoneal cavity (PC) or bronchoalveolar space (BAS) after administration of 1 ml or 100 microl, respectively of saline, glycogen solution (1%) or lipopolysaccharide (LPS 0.1 mg (100 microl)(-1)). Neutrophils were obtained by lavage of both sites with 20 ml saline 24 h after the administration of the stimuli. Glycogen and LPS, depending on the site the cells were obtained from, differently modulated PDG activity. Cells from BAS stimulated by glycogen or LPS had raised PDG activity to 30.5 +/- 5.2 and 42.7 +/- 12.1 nmol min(-1) mg(-1) protein, respectively, when compared with saline (9.1 +/- 0.9 nmol min(-1) mg(-1) protein); mean +/- SEM. On the other hand, cells from PC showed different PDG activity: 52.0 +/- 12.6 nmol min(-1) mg(-1) for saline, 36.5 +/- 9.5 nmol min(-1) mg(-1) for glycogen, and 76.6 +/- 11.2 nmol min(-1) mg(-1) for LPS; mean +/- SEM. Therefore, PDG activity varies with the site from which neutrophils are obtained and the stimulus imposed. The effect of glutamine on nitric oxide (NO) and tumour necrosis factor (TNF) production by peritoneal neutrophils, obtained after glycogen administration, cultured in the presence of LPS (0.5 microg ml(-1)) was also examined. The addition of glutamine at concentrations varying from 2 to 20 mM did not markedly affect NO production. Glutamine alone at 2 mM did not modify the production of TNF but in the presence of LPS caused a significant decrease. So, glutamine may preserve the function of neutrophils during infections and injuries.

Animals↗

PubMed2002

Walker 256 tumour growth causes marked changes of glutamine metabolism in rat small intestine.

The effect of Walker 256 tumour growth on the metabolism of glucose and glutamine in the small intestine of rats was examined. Walker 256 tumour has been extensively used as an experimental model to induce cancer cachexia in rats. Walker 256 tumour growth decreased body weight and small intestine weight and length. The activities of glucose-6-phosphate dehydrogenase and phosphate-dependent glutaminase were reduced in the proximal, median and distal portions of the intestine. Glutamine oxidation was reduced in the proximal portion only. The decrease in glutaminase activity was not due to a low synthesis of the protein as indicated by Western blotting analysis. Hexokinase and citrate synthase activities were not changed by the tumour. These findings led us to postulate that tumour growth impairs glutamine metabolism of small intestine but the mechanism involved remains to be elucidated.

Animals↗

PubMed2002

Incorporation of [1-14C]-linoleic acid by LLC-WRC256 tumour cells.

The incorporation of [(14)C]-linoleic acid (LA) into total lipid fractions was higher in LLC-WRC256 cells from the log phase of growth as compared to those of the plateau phase. LA was mainly incorporated into the phospholipid (PL) fraction of cells during the log phase, whereas in the plateau phase it was mostly taken into cholesterol ester. The proportion of radioactivity was higher in phosphatidylserine of cells from the log phase, whereas in the plateau phase it was higher in phosphatidylcholine. This feature of LA incorporation may be an important factor in determining the proliferative capacity of tumour cells.

Animals↗

PubMed2002

Arachidonic acid cytotoxicity in leukocytes: implications of oxidative stress and eicosanoid synthesis.

Arachidonic acid (AA)-induced cytotoxicity was evaluated in leukocytes: the human leukemia cell lines HL-60, Jurkat and Raji and in rat lymphocytes. Such cytotoxicity was dose- and time-dependent. At concentrations below 5 microM, AA was not toxic; at 10-400 microM, AA induced apoptosis and at concentrations beyond 400 microM, necrosis. The minimum exposure time to trigger cell death was of around 1 h, but the effect was increased by longer exposure times until 6-24 h. Apoptosis was morphologically characterized by a decrease in cell and nuclear volume, chromatin condensation and DNA fragmentation and the presence of lipid bodies, without changes in organelle integrity. Biochemically, AA-induced apoptosis was associated with internucleosomal fragmentation and caspase activation, evaluated by PARP cleavage and the use of a caspase inhibitor. Necrosis was characterized by increased cell volume, presence of loose chromatin, appearance of vacuoles, loss of membrane integrity and of the definition of organelles. The apoptotic effect of AA was studied as to oxidative-reductive imbalance and the participation of eicosanoids. Apoptotic AA treatment was accompanied by an increase in the quantity of thiobarbituric acid reactive substances (TBARS), low-level chemiluminescence and in the glutathione disulfide/reduced glutathione ratio, indicating oxidative stress. The addition of tocopherol, ascorbate, prostaglandin E2 and lipoxygenase inhibitors delayed cell death, whereas the inhibition of cyclooxygenase promoted AA-induced cell death. Cell treatment with AA was accompanied by increased cellular production of LTB4. AA, therefore, is cytotoxic at physiological and supraphysiological concentrations, causing apoptosis and necrosis. Cell treatment with apoptotic concentrations of AA involves oxidative stress and changes in eicosanoid biosynthesis.

Animals↗

PubMed2002

Melatonin inhibits insulin secretion and decreases PKA levels without interfering with glucose metabolism in rat pancreatic islets.

The effect of melatonin (0.1 microM) on freshly isolated islets from adult rats was investigated. Melatonin caused a marked decrease of insulin secretion by islets in response to glucose. The mechanism involved was then examined. Melatonin did not interfere with glucose metabolism as indicated by the measurement of glucose oxidation. However, the content of the protein kinase A (PKA) catalytic alpha-subunit was significantly decreased in islets exposed to melatonin for 1 hr in the presence of 8.3 mM glucose, whereas that of the protein kinase C (PKC) alpha-subunit remained unchanged. Melatonin also inhibited forskolin-induced insulin secretion, a well known activator of adenylate cyclase (AC) activity. This may explain the low content of insulin found in islets incubated in the presence of melatonin for 3 hr. In fact, 3',5' -cyclic adenosine monophosphate (cAMP), a product of AC activity, stimulates insulin synthesis. These findings led us to postulate that a down-regulation of the PKA signaling pathway may be the mechanism involved in the melatonin inhibition of the process of glucose-induced insulin secretion.

Animals↗

PubMed2002

Glutamine plays a role in superoxide production and the expression of p47phox, p22phox and gp91phox in rat neutrophils.

The effect of glutamine on the activity of the NADPH oxidase complex from rat neutrophils was investigated. Superoxide anion (O(2)(-)) production was assessed: (1) by scintillation counting by using lucigenin, and (2) by reduction of cytochrome c over 10 min. The effects of glutamine and PMA on the expression of the NADPH oxidase components p22( phox ), gp91( phox ) and p47( phox ) were also determined. Glutamine at 1 and 2 mM increased O(2)(-) generation in the presence of PMA by 100% and 74% respectively, in neutrophils maintained previously for 3 h in medium deprived of this amino acid. DON (6-diazo-5-oxo-L-norleucine), an inhibitor of phosphate-dependent glutaminase and thus of glutamine metabolism, caused a significant decrease in O(2)(-) production by neutrophils stimulated with PMA both in the absence (44%) and in the presence (66%) of glutamine. PMA markedly increased the expression of gp91( phox ), p22( phox ) and p47( phox ) mRNAs. Glutamine (2 mM) increased the expression of these three proteins both in the absence and in the presence of PMA. We postulate that glutamine leads to O(2)(-) production in neutrophils, probably via the generation of ATP and regulation of the expression of components of NADPH oxidase.

Animals↗

PubMed2002

Effect of diet supplementation with l-carnitine on hepatic catabolism of l-alanine in rats.

AIM: To investigate the effects of chronic supplementation with l-carnitine (LCT) on hepatic catabolism of l-alanine. METHODS: Two groups of male adult Wistar rats were used: 1) supplemented with LCT (1.2 mmol . kg-1 . d-1) dissolved in the drinking water (LCT group) and 2) control group (COG) without LCT supplementation. After one week of LCT supplementation livers from 24 h-fasted rats were perfused in situ and the production of glucose, urea, pyruvate, and l-lactate from l-alanine (5 mmol/L) were measured. RESULTS: LCT decreased the production of glucose and urea from l-alanine. In agreement, pyruvate and l-lactate production from l-alanine were decreased. However, the supplementation with LCT did not show any significant effect on hepatic glucose production from pyruvate (5 mmol/L) and l-lactate (2 mmol/L). CONCLUSION: LCT supplementation decreased the conversion of l-alanine

Alanine↗

PubMedDate not supplied

NBD-cholesterol incorporation by rat macrophages and lymphocytes: a process dependent on the activation state of the cells.

The time-course of incorporation of NBD-cholesterol by macrophages (Ma) and lymphocytes (LY) obtained from untreated and thioglycollate-injected (thio) rats was investigated. NBD-cholesterol incorporation was also examined in Ma obtained from untreated rats and stimulated in vitro by lipopolysaccharide (LPS) and phorbol-myristate acetate (PMA). The same measurement was performed in LY from untreated rats stimulated by addition of LPS and concanavalin A (Con A) into the culture medium. Thio-treated Ma showed high fluorescence intensity after 1 h of incubation with NBD-cholesterol. Ma submitted concomitant to LPS and NBD-cholesterol showed low fluorescence intensity, as well as Ma stimulated with PMA. Ma from untreated and LPS pre-treated rats showed a similar time-course of incorporation. LY from thio-treated rats showed lower incorporation of NBD-cholesterol in comparison to LY from untreated rats. Incorporation was reduced when LPS was added concomitantly with NBD-cholesterol. On the other hand, LY pre-treated with LPS for 48 h showed a very high incorporation of NBD-cholesterol. Con A treatment did not cause a significant effect on NBD-cholesterol incorporation. The findings presented herein led us to conclude that the uptake of NBD-cholesterol by Ma and LY is markedly affected by the activation state of the cells.

4-Chloro-7-nitrobenzofurazan↗

PubMedDate not supplied

Glucose and glutamine utilization by rat lymphocytes, monocytes and neutrophils in culture: a comparative study.

Glucose and glutamine utilization and production of glutamate and lactate were determined for up to 48 h in lymphocytes, monocytes and neutrophils cultured in medium rich in metabolites and vitamins. Glucose was utilized by the three cell types in culture in the following order: neutrophils > monocytes > lymphocytes, whereas lactate was produced in the order: monocytes > neutrophils > lymphocytes. The consumption of glucose followed the activity of glucose-6-phosphate dehydrogenase but it was not related to hexokinase activity. Glutamine was consumed by the three leukocyte types in culture as follows: neutrophils > lymphocytes > or = monocytes. The consumption of glutamine was not fully related to the activity of phosphate-dependent glutaminase. The production of glutamate was not remarkably different among the three cell types. For comparison, glutamine and glucose utilization and glutamate and lactate production were also evaluated using 1-h incubated leukocytes. Under this condition, only glucose or glutamine was added to the medium. Glucose was utilized as follows: neutrophils > monocytes > lymphocytes, whereas lactate was produced in the following order: monocytes > or = neutrophils > lymphocytes. Glutamine was consumed as follows: neutrophils > lymphocytes > monocytes, whereas glutamate was produced as follows: neutrophils > or = monocytes = lymphocytes. The ratio of the amount of glucose/glutamine consumed by 1-h incubated cells was 0.5 for neutrophils, 1.5 for monocytes, and 0.3 for lymphocytes. However, the three cell types cultured for 48 h utilized glucose to a much higher degree than glutamine. The ratio of the amount of glucose/glutamine utilized by the cultured cells was 8.9 for neutrophils, 16.4 for monocytes, and 6.7 for lymphocytes. These observations support the proposition that glutamine is required in much higher amounts than glucose to accomplish the total metabolic requirement of leukocytes. Under conditions closer to physiological when the availability of a variety of metabolites and vitamins is not restricted, glucose is the preferred substrate for lymphocytes, monocytes and neutrophils.

Animals↗

PubMedDate not supplied

The effect of glutamine supplementation on the function of neutrophils from exercised rats.

In a recent publication, we showed the protective effect of glutamine on neutrophil apoptosis induced by acute exercise. The purpose of the present study was to examine the effect of a single bout of intensive exercise on rat neutrophil function and the possible effect of glutamine supplementation. An aqueous solution of glutamine was given by gavage (1 g per kg b.w.), 1 h before the exercise session. The exercise was carried out on a treadmill for 1 h at 85% VO2máx.. Neutrophils were obtained by intraperitoneal lavage with PBS. The following parameters were evaluated: phagocytosis capacity, production of nitric oxide and reactive oxygen metabolites, expression of iNOS, and expression of NADPH-oxidase components (p22phox, p47phox and gp91phox). One hour of exercise at 85% VO2max. induced no change in the phagocytosis capacity and reactive oxygen species production but decreased nitric oxide production. When rats received oral glutamine supplementation, the phagocytosis capacity was significantly increased, the decrease in nitric oxide production induced by exercise was abolished and production of reactive oxygen species was raised. Glutamine supplementation presents a significant effect on neutrophil function including changes induced by exercise.

Animals↗

PubMedDate not supplied

Requirement for glutamine in the expression of alpha-actin and type IV collagen in mesangial cells.

The importance of glutamine for the synthesis of proteins of the extracellular matrix was investigated in cultured mesangial cells. Glutamine at 2 mM elicited an increase in smooth muscle cell alpha-actin, alpha(1)-type IV collagen and fibronectin transcripts (19.0-, 16.7-, and 4.3-fold, respectively) accompanied by an increase in alpha-actin stress fibres compared to cells grown in absence of glutamine. The specificity for the glutamine requirement is suggested by the fact that mRNA levels of tenascin were not altered by addition of glutamine. This suggests that glutamine is required for the expression of important proteins of the extracellular matrix in cultured mesangial cells.

Actins↗

PubMedDate not supplied

Effects of fish oil treatment on bleomycin-induced pulmonary fibrosis in mice.

Bleomycin is an antibiotic used to treat a variety of neoplasms. A major side-effect of bleomycin therapy is the induction of an intense inflammatory response that develops into pulmonary fibrosis. Several studies have shown that certain polyunsaturated fatty acids found in fish oil reduce the inflammatory response in vivo. Fish oil has been employed for the treatment of several pathologies such as glomerulonephritis, cardiovascular diseases, rheumatoid arthritis, and even as an adjuvant in cancer therapy. This study examined the effects of fish oil treatment on the development of bleomycin-induced pulmonary fibrosis. Mice were intraperitoneally treated with bleomycin or with saline daily for 10 days, and 15 days after the last injection they started to receive fish oil by gavage for 14 days. The lungs were processed for light microscopy, biochemical and immunohistochemical investigations. Fish oil did not prevent the development of pulmonary fibrosis after the injury as shown by light microscopy, cytokines immunohistochemical analysis, TBARS content and protein levels in the lung. In addition however, fish oil itself induced a slight inflammatory process in the lung, as observed by the increase in cellularity, vasodilatation in the lung parenchyma, TBARS content, and a slight increase in the lung protein content.

Actins↗