Degeneration Of Renal Tubular Cells Research Articles

Taurine Antioxidant Effect in Decreasing Kidney Damage in Male Mice (Mus Musculus) due to Oxidative Stress Induced by Paraquat

Paraquat toxicity occurs through the high production of reactive oxygen species (ROS) which cause damage due to oxidative stress. Antioxidants can reduce damage through prevention of oxidative stress. Taurine has shown the ability to act as an antioxidant. The aim of this research is to find a effect of antioxidant taurine to decrease kidney damage caused by oxidative stress due to paraquat by looking at the histopathology changes. 25 male adult mices from strain DDY were used and divided into five treatment groups; C(-) (Aquadest IP), C(+) (Paraquat 30mg/kg), P1 (Paraquat 30mg/kg + Taurine 250mg/kg), P2 (Paraquat 30mg/kg + Taurine 500mg/kg) and P3 (Paraquat 30mg/kg + Taurine 1000mg/kg). All groups were given treatment intraperitoneal for twenty one days. The mices were sacrificed where kidney were collected for histopathology preparation. The parameters measured were renal histopathological changes in form of degeneration and necrosis. The results show that taurine administration had an effect on decreased degrees of damage to kidney tubular cells, with a decrease in the mean degree of renal tubular degeneration and necrosis. Degeneration of renal tubular cells in groups (P2) reduced compared to the group (C+) there were significant differences (P <0.05). Necrosis of renal tubular cells in groups (P1, P2) reduced compared to the group (C+) there were significant differences (P <0.05). In conclusion, this research proves that administration of paraquat causes renal histopathological changes which are characterized by degeneration and necrosis. It also proves that taurine dose of 500 mg/kgBB could provided optimal effect.

Pyrethroid-Induced Organ Toxicity and Anti-Oxidant-Supplemented Amelioration of Toxicity and Organ Damage: The Protective Roles of Ascorbic Acid and α-Tocopherol.

The pyrethroid toxicants, fatal at high doses, are found as remnants of crop pesticides and ingredients of commercially available insecticides. The toxic effects of high-content insecticidal pyrethroid formulations are available in 0.05 g, 1.17 g, and 0.04 g pyrethroid-instilled products, namely burning coils, pyrethroid-soaked mats, and liquid formulations of pyrethroids that release pyrethroid vapor/smoke upon heating. They provided 5.46 g/kg, 21.15 g/kg, and 4.24 g/kg of toxicants to the experimental animals over a total of 3 weeks/5 h per os (p.o.) administration, producing necrosis, hyperemia, and fatty changes in the liver; fiber separation in cardiac muscles; atrophy, lymphatic infiltration, blood vessel congestion, and hyperemia in the heart tissues of the experimental animals. The glomerular tuft necrosis, cytoplasmic degeneration of renal tubular cells, necrotic tubules, congestion, and dilatation of blood vessels were observed in the kidney tissue of intoxicated animals. Air-space enlargement, interstitial inflammation, lymphocyte infiltration aggregates, connective tissue infiltration by inflammatory cells, and hyperemia were found in the lung tissues. The pyrethroid toxicants also produced nervous tissue degeneration and decreased neurons in the brain, which were observed through histopathological examinations of the brain, lungs, heart, kidneys, and liver. The protective effects of ascorbic acid (AA/vitamin C) and α-tocopherol (E307/vitamin E) at 100 mg/kg oral doses administered daily for the entire period of the toxicant exposure of three weeks to the experimental mice, aged between 3–4 months and weighing ≈30 g, ameliorated the tissue damage, as observed through the histopathological examinations. The ascorbic acid caused recovery of the liver, kidney, brain, and heart tissue damage, while α-tocopherol was effective at ameliorating the damage in the kidneys and lung tissue compared with the control groups. The high levels of tissue damage recovery suggested a prophylactic effect of the concurrent use of ascorbic acid and α-tocopherol for the subjects under the exposure of pyrethroids.

Fire exposure after lethal hypothermia

A 49-year-old woman was found dead in her apartment after a fire began in her building. During the forensic autopsy, 3rd to 4th degree burns were found on the woman's body, but there were no indications that she was alive when the fire started. Interestingly, hemorrhagic gastric mucosa erosions, as well as bloody contents in the esophagus, stomach, and intestines, were observed. However, the source of the bleeding could not be found. The cause of death was therefore determined to be hypothermia with postmortem fire exposure. The cause of the hypothermia could possibly have been high internal blood loss. The organs showed early signs of putrefaction. It was theorized that the woman had not died immediately before the fire began, but rather a few days before. Examination of heat shock proteins (HSPs) to evaluate premortem thermal influences did not reveal HSP 27, 60, or 70 expression in renal tissue, possibly because of the putrefaction. However, Sudan staining of this tissue revealed a fatty degeneration of renal tubular cells. Opposing temperature influences, as in this case, are rather rare and require thorough investigations.

Toxicologic, hypoglycaemic and hypolipidemic effects of ethanolic and ether extracts of Commiphora molmol from Saudi Arabia

Ether as well as ethanol extracts of Commiphora molmol administered orally to 42 rats at a dose rate of 200, 400 and 600 mg/kg body weight/d for 2 weeks were toxic to laboratory rats. Group 1 was the control which was fed regular diet without the plant extract. Groups 2, 4 and 6 were fed ethanol extract of C. molmol at a dose rate of 200, 400 and 600 mg/kg/body weight/d respectively. Groups 3, 5 and 7 were fed ether extract of C. molmol at a dose rate of 200, 400, 600 mg/kg/body weight/d respectively. The toxic effects were exhibited in all groups by a significant decrease (p<0.05) in the body weights of the experimental rats compared to those weights of the control rats. Experimental animals showed marked depression, abdominal pain, and dyspnoea at their late stages. Haematological changes in rats fed both ether and ethanol extracts of the plant were indicated by significant decrease (p<0.05) in the RBC count as well as in the haemoglobin concentrations while there was significant increase (p<0.05) in the WBC counts. Rats which fed ether extract showed significant decrease in glucose in all groups, cholesterol and triglycerides and a significance increase in bilirubin concentration in experimental animals which fed 400 and 600 mg/body weight/d. Histological changes in experimental rats were observed in the form of fatty change and necrosis of hepatocytes, renal tubular cell degeneration, and shrinkage of the glomeruli.

Alteration of oxidative stress and inflammatory cytokines induces apoptosis in diabetic nephropathy.

Diabetic nephropathy (DN) is one of the most significant long‑term complications in terms of morbidity and mortality for diabetic patients; however, the exact cause remains unknown. To address this, the DN model was established, and oxidative stress indexes, including malondialdehyde (MDA), superoxide dismutase (SOD), glutathione peroxidase (GSH‑Px), and inflammatory cytokines, includinginterleukin‑6 (IL‑6), tumor necrosis factor‑alpha (TNF‑α) and transforming growth factor‑beta (TGF‑β), were examined by ELISA. Renal pathological alterations and cell apoptosis was examined by hematoxylin and eosin and terminal deoxynucleotidyl transferase mediated dUTP nick‑end labeling staining, respectively. The expression levels of B‑cell lymphoma‑2 (Bcl‑2), Bcl‑2 associated X (Bax) and caspase‑3 wereexamined by immunohistochemistry and western blotting. The DN model was correctly established, with lower body weight and the higher blood glucose in the diabetes model group. The expression levels of SOD and GSH‑Px were significantly decreased in the diabetes model group; however, MDA, IL‑6, TNF‑α and TGF‑β were significantly increased. The kidney was severely damaged in the diabetes model group, with inflammatory cell invasion, increasing amount of interstitial matrix and hypertrophy with vacuolar degeneration of renal tubular cells. Cell apoptosis levels were significantly increased, and Bcl‑2 was significantly decreased in the diabetes model group in contrast with that of the sham group; however, Bax and caspase‑3 were significantly increased. It suggested that increased oxidative stress and inflammatory cytokines may enhance the apoptosis levels in DN, and may provide a significant diagnostic reference for DN in diabetes patients.

The kidney in space

Renal adaptation in space has been studied during various space missions since the early 70s. Technical and financial disadvantages of performing experiments under real microgravity conditions have warranted the conductance of relative studies under simulated weightlessness on earth. Arriving in microgravity leads to a redistribution of body fluids to the upper part of the body and an exaggerated extravasation very early in-flight. Plasma volume as well as skin evaporation and oral hydration are reduced, while total body water seems to remain stable. Urinary sodium is diminished and a substantial amount of sodium is retained outside the intravascular space. Glomerular filtration rate shows a transient mild increase. Urinary albumin excretion is reduced although initial studies had demonstrated the opposite. Examination of renal histopathology after exposure to simulated microgravity in rats revealed glomerular atrophy, interstitial edema, and degeneration of renal tubular cells. Acute urinary retention which has been reported during spaceflights can lead to certain medical complications that could compromise an entire mission. Kidney stone formation is another important potential hazard for any manned spaceflight. Increased kidney stone formation in space is attributed to several factors including reduced fluid intake, hypercalciuria, and the presence of nanobacteria. Nutritional and pharmacological interventions are currently recommended as preventive measures against renal stone formation in space travelers.

Linking the metabolism of hydroquinone to its nephrotoxicity and nephrocarcinogenicity.

Hydroquinone (HQ) is nephrocarcinogenic in male Fischer-344 (F344) rats. Kari et al. (1992) described renal tubular cell degeneration in the renal cortex of male F344 rats receiving 1.8 mmol/kg HQ (13 week gavage study) and results from long-term studies demonstrated that HQ exhibited “evidence of carcinogenic activity” in male F344 rats as shown by marked increases in tubular cell adenomas of the kidneys. These findings were confirmed by Shibata et al. (1991), who reported the induction of renal cell tumors in rats following exposure to HQ in the diet (0.8%) for two years. Although the mechanism of HQ-mediated nephrocarcinogencity in male F344 rats is not known, GSH conjugates of HQ may play an important role. We have previously shown that multi-substituted glutathione (GSH) conjugates of HQ cause selective necrosis of renal proximal tubule cells in Sprague-Dawley rats when administered by intravenous injection, with 2,3,5-(triGSyl)HQ being the most potent nephrotoxicant (Lau et al., 1988). Furthermore, HQ-GSH conjugates have been identified as both in vitro and in vivo metabolites of HQ in the Sprague-Dawley rat, in quantities sufficient to propose a role for GSH conjugation in the nephrotoxicity of HQ (Hill et al., 1993). In the present study we investigated the metabolism of [14C]-HQ to HQ thioethers in the F344 rat, the rat strain used in the carcinogenicity studies, and also examined the effect of subchronic administration on the elimination and metabolic profile of [14C]-HQ. We propose that the formation of nephrotoxic metabolites may play a role in HQ-induced nephrocarcinogenicity by a mechanism that involves the generation of reactive oxygen species, oxidative DNA damage, and cytotoxicity followed by sustained hyperplasia.KeywordsRenal Cell TumorPotassium BromateRenal Proximal Tubule CellSubchronic AdministrationThymine GlycolThese keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

Tubulointerstitial nephritis induced by Tamm-Horsfall protein sensitization in guinea pigs

Experimental tubulointerstitial nephritis (TIN) was induced in guinea pigs by immunization with homologous Tamm-Horsfall protein (THP). This disease was characterized by focal interstitial mononuclear cell infiltration around the distal nephron segments with degeneration of renal tubular cells. Although concomitant granular immunoglobulin deposition on the tubular basement membrane and a rise of serum anti-THP antibodies were recognized, they were related to the severity of the lesion. Lymphocytes from lymph nodes of animals with TIN showed blast transformation in the presence of THP in vitro. Following the transfer of lymphocytes and spleen cells from guinea pigs with THP-induced TIN to nonimmunized animals, the recipient animals developed TIN 7 days later. These observations suggest that TIN induced in guinea pigs by challenge with homologous THP may, at least in part, be related to a cell-mediated immune response.

Pentachlorophenol poisoning in a nursery for newborn infants. I. Clinical features and treatment

Nine neonates, all born in the same hospital, presented with a syndrome characterized by excessive sweating, tachycardia, tachypnea, respiratory distress, hepatic enlargement, and metabolic acidosis. Two of these infants died. The clinical condition of the first infant seen with this syndrome deteriorated rapidly and he died; the autopsy revealed fatty infiltration of the liver and fatty degeneration of renal tubular cells. Six subsequent patients who presented with severe manifestations of the illness were subjected to exchange blood transfusion and in each instance there was a dramatic improvement following this therapy. All 6 infants survived, as did a seventh infant who recovered with only supportive therapy. The second death occurred in an infant in whom the clinical condition deteriorated so rapidly that exchange transfusion could not be performed. Subsequent investigation revealed that 11 additional infants had been affected with a similar but milder illness and that the syndrome had been produced by the percutaneous absorption of pentachlorophenol which had been used in the laundering of the diapers and the infants' bed linen.