Biomedical subjects

Chau-Fong Chen

Publications and source records attributed to Chau-Fong Chen.

14 recordsLinked to original sources

PubMed2003

Changes in renal hemodynamics and urodynamics in rats with chronic hyperoxaluria and after acute oxalate infusion: role of free radicals.

AIMS: The aim of this study was to evaluate possible changes in renal hemodynamic and urodynamic parameters in rats with chronic hyperoxaluria and after acute oxalate challenge. We also evaluated the possible association between free radical (FR) production, hyperoxaluria, and calcium oxalate (CaOx) calculi formation. METHODS: Chronic hyperoxaluria was induced by adding 0.75% ethylene glycol (EG) to the drinking water of male Wistar rats. After 7, 21, and 42 days of treatment, urinary biochemistry, oxalate levels, and lipid peroxides were measured. Kidney calculi were examined by polarizing microscopy. In the second part of the experiments, 1, 10, 20, and 30 mg kg(-1) hr(-1) oxalate was infused, by means of an intrarenal arterial catheter (IRA), into normal rats sequentially. Superoxide dismutase (SOD) infusion by means of IRA, in addition to oxalate, was also performed to check its influence on the altered renal function after oxalate infusion. In both the acute and chronic groups, renal blood flow (RBF), cortical microvascular blood flow (CMVBF), glomerular filtration rate (GFR), urine flow (UV), and urinary sodium excretion (U(Na)V) were measured, and chemiluminescence (CL) was examined in the renal venous blood. RESULTS: Levels of urinary lipid peroxides and enzymuria had increased since day 7, and increased the size of numbers of CaOx crystals in the kidney were noted beginning on day 21, but elevated CL was detectable only on day 7 after 0.75% EG treatment. Decreased UV and U(Na)V were noted in the 42-day EG group, although the 24-hr creatinine clearance values were normal in all experimental groups. On the other hand, RBF, GFR, and CMVBF were attenuated with elevated FR when the oxalate concentration was higher than 10 mg kg(-1) hr(-1) in the acute oxalate infusion group. With SOD pretreatment, the decreased RBF, GFR, and CMVBF could be reversed at 10 mg kg(-1) hr(-1) of oxalate, and be partially reversed at 20. FR also could be reduced significantly at 10 and 20 mg kg(-1) hr(-1) of oxalate. CONCLUSIONS: Decreased urine flow and sodium excretion were the main renal functions affected by chronic hyperoxaluria. However, that only the 42-day EG group had a decreased tubular function cannot be fully explained by the persistent tubular enzymuria and increased lipid peroxides that began on day 7 after EG treatment. With acute oxalate infusion, the major insult to renal function was renal hemodynamics. Pretreated SOD could reverse the attenuated hemodynamics and reduce the elevated FR partly, which suggested that FR is responsible for oxalate toxicity.

Acute Disease↗

PubMed2003

The effect of an intestinal ischemia-reperfusion injury on renal nerve activity among rats.

An intestinal ischemia-reperfusion injury (IIR) may induce renal tubular dysfunction and a reduction in renal blood flow that may be related to the alteration of renal-nerve activity. A rat model of IIR injury was established. The superior mesenteric artery was clamped for 120 min, constituting the ischemic period, and was then released for 60 min, thus constituting the reperfusion period. Renal-nerve activity, renal function, and hemodynamic changes were recorded during the different periods. The levels of calcitonin gene-related peptide (CGRP) in portal-vein blood and intestinal tissue were investigated here. In the reperfusion period, the efferent renal-nerve activity (ERNA) was markedly elevated (94.3% +/- 21.6% higher than the baseline value), such an elevation being only partially reversed by fluid expansion (29.3% +/- 5.2% higher than the baseline value). The elevation of ERNA contributed to the renal blood-flow reduction from 6.8 +/- 0.3 mL/min/g to 2.0 +/- 0.4 mL/min/g, and decreased diuretic and natriuretic responses. The afferent renal nerve activity (ARNA) was markedly depressed (45.7% +/- 8.1% lower than the baseline value) during the reperfusion period. This depression was not reversed by fluid expansion, suggesting that the baroreflex was not responsible for this effect. The blunted ARNA also contributed to the elevation of ERNA by way of a renorenal reflex. The potent vasodilator neuropeptide in the gut, CGRP, revealed an increased level in the portal-vein blood (92.2 +/- 4.4 pg/mL vs. 57.8 +/- 0.6 pg/mL) and also in intestinal tissue (655.8 +/- 115.9 pg/mL vs. 60.5 +/- 9.4 pg/mL) with a time-matched related pattern with the change to renal-nerve activity, suggesting CGRP's role regarding changes in renal-nerve activity. This study indicates that the elevated ERNA level associated with IIR injury is related to a systemic hypotension-induced baroreflex, the contra-lateral inhibition of ARNA, and possibly also gut-released CGRP. In regards to an IIR injury, the depressed ARNA reflects the involvement of a renal sensory- impairment mechanism.

Afferent Pathways↗

PubMed2003

Hypoxic preconditioning prevents cortical infarction by transient focal ischemia-reperfusion.

One of the proposed pathologic actions underlying brain infarction is excess free radicals resulting from reoxygenation. In this paper we report an investigation of the neuroprotective effect of hypoxic preconditioning on transient focal ischemia-reperfusion injuries in rat brain. Female Wistar rats were subjected to 380 mmHg in an altitude chamber for 15 hours/day. Our ex vivo studies showed that auto-oxidation and iron-induced lipid peroxidation of brain homogenates of the four-week hypoxia-preconditioned rats were significantly lower than those of the normoxic rats. A focal infarction in the cerebral cortex of normoxic rats was consistently observed 24 hours after a 60-minute transient ischemic occlusion of the right middle cerebral artery and bilateral common carotid arteries. Hypoxic preconditioning in fact attenuated cortical infarction in a duration-dependent manner. Induction of the neuroprotection required two weeks of hypoxic preconditioning. Four weeks of hypoxic preconditioning significantly reduced the cortical infarcted area, the elevated lipid peroxidation, and resulted in an acute increase in cytosolic cytochrome c in the infarcted cortex of normoxic rats. The protective effect of four weeks of hypoxic preconditioning lasted seven days under a renormoxic condition. Our data suggest that oxidative stress may result in apoptosis in the transient focal ischemia-reperfusion injuries. Furthermore, hypoxic preconditioning attenuated cortical infarction in the rat brain. Although supplementation of antioxidants may encounter difficulty at the blood-brain barrier, hypoxic preconditioning is very likely to protect CNS targets from oxidative injuries without any barrier.

Animals↗

PubMed2003

Fluid administration prevents renal dysfunction during hypotension under spinal anesthesia in a rat model.

BACKGROUND: Severe hypotension deteriorates renal functions and renal hemodynamics especially renal cortical blood flow. Systemic hypotension following high level spinal anesthesia may impair renal functions in spite of the blockade of renal sympathetic nerves that may help prevent vasoconstriction. Fluid loading is clinically applied for preventing hypotension but the effects on the changes of renal functions have not been studied. This study was designed to investigate the effects of fluid loading on systemic hemodynamics, renal hemodynamics and functions especially the blood distribution to renal cortex. METHODS: A rat model was used in our study. Intravenous normal saline infusion was started in both control group (5 ml/kg/h, 8 rats) and fluid loading group (15 ml/kg/h, 8 rats) 30 min before spinal anesthesia. A high level (above T4) spinal anesthesia was conducted via a preset intrathecal catheter with 0.5% hyperbaric bupivacaine. Blood pressure, heart rate and renal cortical microvascular blood flow (CMBF) were measured via a laser Doppler probe firmly contacted on renal cortex and recorded continuously after spinal anesthesia. Renal functions including glomerular filtration rates (GFR, by inulin clearance), effective renal plasma flow (ERPF, by P-aminohippurate clearance), urine flow rate (UFR) and electrolytes excretion were measured every 30 min after spinal anesthesia. RESULTS: Severe hypotension was notable within 5-10 min after intrathecal anesthesia and recovered with 30 min in both groups but the difference was not significant between groups. In the control group, GFR and ERPF decreased significantly in the first 30 min by 51.9 +/- 19.8% and 44.3 +/- 13.7% respectively (P < 0.05) and recovered after 60 min. Also the deteriorations of UFR and CMBF were significantly longer (over 60 min). In fluid loading group, ERPF, UFR and CMBF could maintain throughout the experiment but only GFR was affected in the first 30 min. CONCLUSIONS: Fluid administration did not prevent hypotension following high level spinal anesthesia but might have beneficial effects on renal hemodynamics especially on the renal cortical circulation and urine flow rate.

Anesthesia, Spinal↗

PubMed2002

Simple methods to elevate pulmonary arterial pressure by pre- and post-tricuspid shunts in rats.

BACKGROUND: Arteriovenous shunt in the rat is an extremely useful experimental animal model for investigating cardiac hypertrophy as well as the hemodynamics and endocrine aspects of chronic heart failure. AIMS: The present study was to develop 2 pre-tricuspid and 1 post-tricuspid models of arteriovenous shunt to induce right ventricular hypertrophy and increase pulmonary blood flow in growing rats. METHODS: In the first model, an arteriovenous shunt was created from the common iliac artery to the inferior vena cava (ICS). The second model was shunted from the common carotid artery to the external jugular vein (CJS). A post-tricuspid shunt (the third model) was made by introducing the right common carotid artery into the right ventricular outflow tract (CVS). RESULTS: Four weeks after the shunt surgery, the pulmonary artery pressure was 14.4 +/- 0.5 mmHg in the control group, 15.8 +/- 0.8 mmHg in the ICS group, 21.2 +/- 0.7 mmHg in the CJS group, and 20.2 +/- 1.1 mmHg in the CVS group. The percentage of increasing pulmonary blood flow was 33.0 +/- 1.0% in the CJS group and 26.9 +/- 1.3% in the ICS group four weeks after shunt operation. The oxygen partial pressure of pulmonary artery blood was 30.9 +/- 0.7 mmHg in the control group, 33.6 +/- 1.0 mmHg in the ICS group, 43.7 +/- 1.4 mmHg in the CJS group and 41.1 +/- 2.5 mmHg in the CVS group. The CJS and CVS groups had significant right ventricle hypertrophy. CONCLUSIONS: These three models can provide for study of the flow-pressure effect of the right heart and pulmonary circulation.

Animals↗

PubMed2002

Enhanced expression of nitric oxide synthase in the early stage after increased pulmonary blood flow in rats.

OBJECTIVE: Evidence that vasodilator nitric oxide mediates normal pulmonary vascular tone has led to the hypothesis that endothelial injury induced by congenital heart disease with increased pulmonary blood flow disrupts these regulatory mechanisms and its associated altered vascular reactivity. Therefore, we hypothesized that increased pulmonary blood flow results in altered expression of endothelial nitric oxide synthase (eNOS). METHODS: We created an arteriovenous shunt in female Wistar (5-week-old) and measured the change of pulmonary blood flow and pressure immediately after and 1 month after the shunt operation. The protein levels of eNOS in the lung tissues of rats were assessed. RESULTS: The shunt immediately resulted in a significant increase in pulmonary blood flow (16.5 +/- 11.8% , pulmonary artery pressure (2.3 +/- 0.7 mm Hg), and blood O(2) saturation (16.1 +/- 11.8%) in the pulmonary artery. After 4 weeks, there was a significant increase in pulmonary blood flow (30.7 +/- 1.6%), pulmonary artery pressures (4.3 +/- 1.1 mm Hg), and blood O(2) content (43.3 +/- 17.5%). Western blot analysis demonstrated that eNOS protein was increased in the shunt lung 72 h after surgery and recovered to the control level 1 week later. CONCLUSION: This simple shunt model can induce early upregulation of eNOS expression with increased pulmonary blood flow and pulmonary artery pressure in rats.

Analysis of Variance↗

PubMed2002

Melatonin attenuates the neuronal NADPH-d/NOS expression in the nodose ganglion of acute hypoxic rats.

Excessive production of nitric oxide (NO) may play a detrimental role in the process of hypoxia-related neuropathology. This study explored whether treatment with melatonin would attenuate the neuropathological changes in the vagal ganglia following a severe hypoxic insult. Thirty minutes prior to hypoxia treatment, young adult rats were pre-treated with melatonin at 5. 25 or 100 mg/kg injected intraperitoneally. Hypoxia was achieved by subjecting the rats to a barometric pressure of 0.2 atm (PO2 = 43 Torr) for 4 hr in an altitude chamber. Nicotinamine adenine dinucleotide phosphatediaphorase (NADPH-d) histochemistry combined with the neuronal nitric oxide synthase (nNOS) immunohistochemistry were used to detect the NADPH-d/nNOS reactivity in the nodose ganglion (NG) at various time points following the hypoxic exposure. In normal untreated rats, about 43% of the neurons in the NG displayed NADPH-d/nNOS reactivity. Following hypoxic exposure, both the percentage and the staining intensity of NADPH-d/nNOS positive neurons in the NG were markedly increased, but these were reduced in longer surviving animals. Quantitative analysis of cell counts revealed that about 17% of the neurons died at 14 days after hypoxia treatment. However, in hypoxic rats given different doses of melatonin pretreatment, neuronal death as well as the frequency and staining intensity of NADPH-d/nNOS reactivity of the nodose neurons were significantly decreased. The effect of melatonin on neuronal survival and NADPH-d/ nNOS expression was dose-dependent. It is therefore suggested that melatonin exerts a neuroprotective effect and may serve as a potential therapeutic strategy for prevention and/or reducing the susceptibility of nodose neurons to NO-mediated hypoxic neuropathy.

Animals↗

PubMed2002

Small-dose propofol sedation attenuates the formation of reactive oxygen species in tourniquet-induced ischemia-reperfusion injury under spinal anesthesia.

UNLABELLED: The release of a tourniquet produces reactive oxygen species (ROS), which can cause ischemia-reperfusion injury. We investigated the effects on ROS production in 22 adult ASA physical status I-II patients sedated with small-dose propofol infusion and IV midazolam undergoing elective total knee replacement under intrathecal anesthesia, allocated randomly to one of two groups. In the Propofol group, sedation was performed with propofol 0.2 mg/kg followed by infusion at a rate of 2 mg. kg(-1). h(-1). In the Control group, IV midazolam 5 mg was given. ROS production was measured by lucigenin chemiluminescence analysis. Blood samples were obtained from the radial artery after spinal anesthesia, 1 min before release of the tourniquet and 5 and 20 min after reperfusion. The ischemic time was approximately 70 min. ROS production decreased nonsignificantly before reperfusion in both groups but increased significantly 5 and 20 min after reperfusion in the Midazolam group. In the Propofol group, no significant increase of ROS production was found. We conclude that small-dose propofol infusion attenuates ROS production in tourniquet-induced ischemia-reperfusion injury. IMPLICATIONS: Small-dose propofol sedation, compared with IV midazolam, attenuates free radical production after release of the tourniquet during total knee replacement under spinal anesthesia.

Aged↗

PubMed2002

Impaired renal sensory responses after renal ischemia in the rat.

Renal sensory responses and reflex function were examined in rats 24 h after 45 min of ischemic injury caused by unilateral renal arterial occlusion (RAO). The integrity of renal pelvic mechanoreceptor (MRu)-mediated renorenal reflex was examined. An increase in ipsilateral afferent renal nerve activity (ARNA) and a reflex decrease in efferent renal nerve activity (ERNA) and contralateral diuresis and natriuresis produced by increasing the intrapelvic pressure were seen in sham-operated (Sham) rats, but it was largely attenuated in RAO rats. Using single-fiber recordings of the renal MRu discharge, graded increases in intrapelvic pressure or renal pelvic administration of substance P (SP) resulted in pressure- or concentration-dependent increases in ARNA in the control kidney of Sham rats, whereas attenuated responses were seen in the postischemic kidney of RAO rats. The unresponsiveness of renal MRus in RAO rats was accompanied by an insufficient release of SP. However, the baseline SP release is higher in RAO kidneys due to a reduced neutral endopeptidase (NEP) activity in the renal pelvis of the postischemic kidney. No changes in NK-1 receptor mRNA levels were demonstrated; however, the expression of NK-1 receptors in the plasma membrane of RAO pelvis were decreased, possibly resulting from the internalization of the receptors associated with beta-arrestin trafficking. Renal excretory responses after saline loading were significantly lower in the postischemic kidney of RAO rats than in Sham rats. Responses of ARNA and ERNA were also lower. It is concluded that the defective activation of renal sensory mechanoreceptors in the postischemic kidney results from an inadequate release of SP after mechanostimulation and the reduced functional NK-1 receptors.

Animals↗

PubMed2002

Temporal increase in the reactivity of pulmonary vasculature to substance P in chronically hypoxic rats.

We previously demonstrated that the pulmonary vascular response to substance P (SP) increased in chronically hypoxic rats. This study explored the temporal increase in reactivity of the pulmonary vascular response to SP and its underlying mechanisms. First, young female Wistar rats were exposed to sea level (SL) or simulated high altitude (HA) for 15 h/day for 3 days, 1 wk, 2 wk, and 4 wk. Lungs were isolated and perfused with 4% bovine serum albumin in Krebs-Henseleit buffer solution. SP (1.5 x 10(-4) M) induced significant increases in pulmonary arterial pressure (P(pa)), venous pressure (P(v)), capillary pressure (P(c)), arterial resistance (R(a)), and filtration coefficient (K(fc)) in SL lungs. Increases in P(pa) and R(a) were significantly augmented in HA lungs, with a temporal increase trend peaking at 2 wk of HA exposure. The selective neurokinin (NK) type 1 (NK1) receptor antagonist SR-14033 significantly attenuated SP-induced increases in P(pa), P(v), P(c), R(a), and K(fc) in SL lungs. In lungs exposed to HA for 2 wk, SR-14033 suppressed the effect of SP on P(pa). Also, chronic hypoxia induced significant increases in NK1 receptors and NK1 receptor mRNA, with a temporal trend. We conclude that chronic hypoxia temporally augments SP-induced vascular responses, which are closely associated with increases in NK1 receptors and gene expression.

Altitude↗

PubMed2002

Temporal decrease in renal sensory responses in rats after chronic ligation of the bile duct.

Renal responses to renal sensory receptor activation were examined in rats after 1 and 4 wk of common bile duct ligation (CBDL). Compared with sham-operated rats (Sham), urine and sodium excretion after acute saline loading was significantly reduced at both times after CBDL. The blunted excretory responses in CBDL rats, accompanied by less activation of afferent renal nerve activity (ARNA), were already apparent at 1 wk and became severe at 4 wk. The defect in ARNA activation in CBDL rats was further studied using specific stimuli to activate renal sensory receptors. Graded increases in intrapelvic pressure or renal pelvic perfusion of substance P (SP) elicited an increase in ARNA in Sham rats, these responses being temporally attenuated in CBDL rats. Despite no significant change in renal pelvic SP release, no renorenal reflex was demonstrable in 4-wk CBDL rats. Immunoblotting showed that expression of renal pelvic neurokinin 1 (NK-1) receptors was 32 and 47% lower in 1- and 4-wk CBDL rats, respectively, than in Sham rats, this decrease correlating well with plasma SP levels. The quantitative real-time RT-PCR showed similar levels of NK-1 receptor mRNA in the renal pelvis in the Sham and 4-wk CBDL groups. We conclude that impairment of renal excretory and sensory responses increases with the duration of cirrhosis. An impaired renorenal reflex in cirrhotic rats is involved in the defective activation of the renal sensory receptors could be due, in part, to the low expression of NK-1 receptors, which is dependent on the duration of CBDL. The decrease in NK-1 receptor protein levels is not due to a decrease in mRNA levels.

Animals↗

PubMed2002

Impaired renal sensory responses after unilateral ureteral obstruction in the rat.

Renal responses to the activation of renal sensory receptors were examined in rats after release of 24-h unilateral ureteral obstruction of the left kidney. The integrity of the renorenal reflex was examined in both 24-h unilateral ureteral obstruction-treated (UUO) and sham-operated (Sham) rats. Increased ipsilateral afferent renal nerve activity (ARNA) and reflexly decreased efferent renal nerve activity (ERNA) and increased contralateral diuresis and natriuresis produced by increasing the left intrapelvic pressure were observed in Sham rats but not in UUO rats. The lack of responsiveness of the renorenal reflex in UUO rats was associated with lower release of substance P (SP) and increased neutral endopeptidase (NEP) activity in the renal pelvis in the postobstructive kidney. Compared with Sham rats, urine and sodium excretion after acute saline loading was significantly reduced in the postobstructive kidney. The blunted excretory responses were accompanied by lower activation of ARNA and less reflex inhibition of ERNA. Renal sensory dysfunction in the postobstructive kidney was further examined by stimulation of renal mechanoreceptors and chemoreceptors. Graded increases in intrapelvic pressure or renal pelvic perfusion with hypertonic saline solution elicited, respectively, a pressure- or concentration-dependent increase in ARNA in the control kidney of Sham rats, this response being greatly attenuated in the postobstructive kidney. Western blots showed no quantitative difference in the expression of renal pelvic neurokinin 1 (NK-1) receptors between the two groups. It was concluded that renal sensory function is impaired in the postobstructive kidney of UUO rats and that this defective activation of renal sensory receptors results in an impaired renorenal reflex, which is associated with enhanced NEP activity and catabolism of SP released in the renal pelvis and is not related to the expression of NK-1 receptor protein.

Afferent Pathways↗

PubMed2002

Changes in the oxidant-antioxidant balance in the kidney of rats with nephrolithiasis induced by ethylene glycol.

PURPOSE: We investigated the possible mechanism of increased free radicals, the role of antioxidant enzymes and their correlation with renal tubular damage in the kidney after feeding 0.75% ethylene glycol to male Wistar rats. MATERIALS AND METHODS: Rats were divided into 7 experimental groups according to the duration of ethylene glycol feeding (1, 3, 5, 7, 9, 21 or 42 days) and into age matched control groups. Chemiluminescence levels were examined in blood samples (renal artery and vein) and in the kidney. The activities of oxidase and antioxidant enzymes were measured in kidney homogenates. The nitroblue tetrazolium perfusion method and immunohistochemical stains with ED1 and CD45 were performed. Urinary levels of alpha and mu-glutathione S-transferase (GST) were also measured and expressed in gm. urinary creatinine. RESULTS: Chemiluminescence levels of renal venous blood samples were elevated on days 1, 3 and 7 (p <0.05), and those of the kidney were elevated only on days 3 and 42 (p <0.05) compared with controls. The infiltration of CD45 positive cells in the kidney increased on day 7 and a further increase in these positive cells was noted on day 21. Fused ED1 positive cells surrounding the calcium oxalate crystals and adjacent to the nitroblue tetrazolium positive area were found on day 42. Xanthine oxidase activity showed no significant change, whereas nicotinamide adenine dinucleotide dependent oxidase activity was higher on day 5 and nicotinamide adenine dinucleotide phosphate dependent activity was elevated in all experimental groups (p <0.05). The activities of catalase and manganese superoxide dismutase were elevated in the early stage. On day 42 almost all antioxidant enzyme activities were attenuated (p <0.05) except that of catalase. The urinary levels of alpha-GST were elevated from day 7 until day 42, whereas levels of mu-GST were elevated from day 3 until day 42 except day 5. CONCLUSIONS: The possible mechanism that causes free radical elevation in the kidney may be different in the course of nephrolithiasis after ethylene glycol treatment. Initially the systemic circulation may bring the toxic substance into the kidney and cause it to produce free radicals. In the late stage gradually infiltrating leukocytes and decreased antioxidant enzyme activities may cause the kidney to remain under excessive oxidative stress.

Animals↗

PubMed2001

De novo demonstration and co-localization of free-radical production and apoptosis formation in rat kidney subjected to ischemia/reperfusion.

Ischemia-induced oxidative damage to the reperfused kidney was examined. A modified chemiluminescence method, an in situ nitro blue tetrazolium perfusion technique, and a DNA fragmentation/apoptosis-related protein assay were adapted for demonstration de novo and co-localization of reactive oxygen species (ROS) production and apoptosis formation in rat kidneys subjected to ischemia/reperfusion injury. The results showed that prolonged ischemia potentiated proapoptotic mechanisms, including increases in the Bax/Bcl-2 ratio, CPP32 expression, and poly-(ADP-ribose)-polymerase fragments, and subsequently resulted in severe apoptosis, including increases in DNA fragmentation and apoptotic cell number in renal proximal tubules (PT) and distal tubules (DT) in a time-dependent manner. The increased level of ROS detected on the renal surface was correlated with that in blood and was intensified by a prolonged interval of ischemia. The main source of ROS synthesis was the PT epithelial cells. The ROS and apoptotic nuclei detected in the PT cells can be ameliorated by superoxide dismutase (SOD) treatment before reperfusion. However, the apoptotic nuclei remained in DT in the SOD-treated rats, indicating that formation of apoptosis in DT was not influenced by the small amounts of ROS produced. In PT and DT cell cultures, significant increases in apoptotic cells and ROS were evident in PT cells after hypoxia/reoxygenation insult. Furthermore, the oxidative damage in PT, but not in DT, can be alleviated by ROS scavengers SOD and hexa(sulfobutyl)fullerene, confirming that PT are vulnerable to ROS. These results lead us to conclude that ROS produced in significant amounts in PT epithelium under ischemia/reperfusion or hypoxia/reoxygenation conditions may be responsible for the apoptotic death of these cells.

Animals↗