Kidney Of Male Rats Research Articles

Protective Effect of Platelet-Rich Plasma on Cisplatin-Induced Nephrotoxicity in Adult Male Albino Rats: Histological and Immunohistochemical Study.

Cisplatin is a potent antineoplastic drug that is used for treatment of many solid tumors. It has a wide range of adverse effects. Nephrotoxicity is the most common one of them. Platelet-rich plasma (PRP) is an autologous human plasma that activates the tissue regeneration through cell proliferation and differentiation. Study the role of PRP in amelioration of cisplatin-induced nephrotoxicity on the kidney of adult male albino rats by biochemical, morphometric, histological, and immunohistochemical studies. Thirty-five adult male albino rats were used. Thirty rats were included as experimental group and five were used to obtain the PRP. The experimental group was classified into as follows: control group which received 1mL of sterile saline by intraperitoneal injection (IP), cisplatin-treated group which received cisplatin 7.5 mg/kg IP in a single dose and cisplatin and PRP-treated group rats received cisplatin 7.5 mg/kg single IP dose followed by 1ml of PRP IP after 24 h of cisplatin injection. There was a significant increase in urea and creatinine levels in cisplatin-treated group in comparison to the control and the PRP groups. The kidneys of cisplatin-treated group showed distorted renal structure, where specimens of PRP-treated group revealed restoration of the classical appearance of the renal tissue similar to the control group. PRP has protective effects on renal structure and functions and it helps to ameliorate the histological changes induced by cisplatin.

Study the Effect of Selenium Supplementations on the Liver, Kidney and Thyroid Gland Activities in Male Rats

The liver, kidney, and thyroid glands are main vital in biochemical and physiological activities in animals and humans. In this study, we examined the effects of adding selenium supplementation on the improvement activity of many glands such as the liver, kidney, and thyroid after cadmium chloride administration (induced toxicity) in male rabbits. This study included 16 male rabbits divided into four groups, the 1st group (CON) was control and administration normal fed and drinking water, the 2nd group (NC ) was negative control group that administration of 1ml of cadmium chloride (100ppm) with normal fed, the 3rd group (S1) was administration of 1ml of sodium selenite, and 4th group (S2) was administration of 5ml of selenium and all groups continuous for same style up to 8th week of experiment. Antioxidant and oxidative stress status was investigated by measuring the levels of T-AOC and MDA. The liver was assessed by estimation of ALT, AST, TP, and TB while kidney was assessed by calculation of blood CRI and UR and the thyroid gland assessed by measurement of serum T3 and T4. The levels of selenoprotein (SeP) mg/l were assessed by HPLC for standard and S2 group. The results of present study shows highly statistical differences between four group when compare the mean±SD of the levels of ALT,AST,TP,TB,CRI,UR,T3, and T4 (p-value <0.005). In conclusion, this study showing highly ability of selenium supplementation to lowering the levels of the markers of liver, kidney, and thyroid gland and work as protective factor from toxicity induced by cadmium in male rabbits.

Effect of sub-dermal exposure of silver nanoparticles on hepatic, renal and cardiac functions accompanying oxidative damage in male Wistar rats

Silver nanoparticles (AgNPs) have been generally used due to their strong antibacterial, antiviral and antifungal and antimicrobial properties. However, their toxicity is a subject of sustained debate, thus requiring further studies. Hence, this study examines the adverse effects of the sub-dermal administered dose of AgNPs (200 nm) on the liver, kidney and heart of male Wistar rats. Thirty male rats were randomly distributed into six groups of five animals per group. Group A and D served as the control and received distilled water for 14 and 28 days respectively. Groups B and C were sub-dermally exposed to AgNPs at 10 and 50 mg/kg daily for 14 days while E and F were sub-dermally exposed to AgNPs at 10 and 50 mg/kg daily for 28 days. The liver, kidney and heart of the animals were collected, processed and used for biochemical and histological analysis. Our results revealed that the subdermal administration of AgNPs induced significant increased (p < 0.05) activities of aspartate aminotransferase (AST), alanine transferase (ALT), alkaline phosphatase (ALP), urea, creatinine, and malondialdehyde (MDA) while decreasing the levels of glutathione (GSH), catalase (CAT), superoxide dismutase (SOD), and total thiol groups in the rat tissues. Our findings suggest that the subdermal administration of AgNPs induced oxidative stress and impaired the hepatic, renal and cardiac functions of male Wistar rats.

Gut Microbiota Perturbation in Early Life Could Influence Pediatric Blood Pressure Regulation in a Sex-Dependent Manner in Juvenile Rats.

The present study aimed to investigate whether gut dysbiosis induced by ceftriaxone in early life could influence pediatric blood pressure regulation in childhood with or without exposure to a high-fat diet (HFD). Sixty-three newborn pups of Sprague-Dawley rats were administered ceftriaxone sodium or saline solution until weaning at 3 weeks, and the rats were fed a HFD or regular diet from 3 to 6 weeks. Tail-cuff blood pressure, the expression levels of genes of the renin-angiotensin system (RAS), the concentrations of IL-1β, IL-6, and TNF-α in the colon and prefrontal cortex, and the composition of fecal microbiota were analyzed. Ceftriaxone treatment significantly increased the diastolic blood pressure of male rats at 3 weeks. At 6 weeks, systolic blood pressure (SBP) was significantly increased only in ceftriaxone treated male rats fed with HFD. The RAS showed increased activation in the kidney, heart, hypothalamus, and thoracic and abdominal aorta of male rats, but only in the kidney, heart, and hypothalamus of female rats. HFD-fed female rats showed a decreased level of IL-6 in the colon. α diversity of gut microbiota decreased and the Firmicutes to Bacteroidetes ratio increased in both male and female rats at 3 weeks; however, these parameters recovered to various degrees in female rats at 6 weeks. These results revealed that early-life gut dysbiosis induced by antibiotics combined with a HFD in childhood could be involved in pediatric blood pressure regulation and an increase in SBP in juvenile rats, and these effects occurred in a sex-dependent manner.

Combined cerium and zinc oxide nanoparticles induced hepato-renal damage in rats through oxidative stress mediated inflammation

The toxicity profiles of nanoparticles (NPs) used in appliances nowadays remains unknown. In this study, we investigated the toxicological consequences of exposure to cerium oxide (CeO2) and zinc oxide (ZnO) nanoparticles given singly or in combination on the integrity of liver and kidney of male Wistar rats. Twenty (20) rats were allotted into four groups and treated as: Control (normal saline), CeO2NPs (50 μg/kg), ZnONPs (80 μg/kg) and [CeO2NPs (50 μg/kg) + ZnONPs (80 μg/kg)]. The nanoparticles were given to the animals through the intraperitoneal route, three times per week for four repeated weeks. Results revealed that CeO2 and ZnO NPs (singly) increased serum AST and ALT by 29% & 57%; 41% & 18%, and co-administration by 53% and 23%, respectively. CeO2 and ZnO NPs increased hepatic and renal malondialdehyde (MDA) by 33% and 30%; 38% and 67%, respectively, while co-administration increased hepatic and renal MDA by 43% and 40%, respectively. The combined NPs increased hepatic NO by 28%. Also, CeO2 and ZnO NPs, and combined increased BAX, interleukin-1β and TNF-α by 45, 38, 52%; 47, 23, 82% and 41, 83, 70%, respectively. Histology revealed hepatic necrosis and renal haemorrhagic parenchymal in NPs-treated rats. Summarily, CeO2 and ZnO NPs produced oxidative injury and induced inflammatory process in the liver and kidney of experimental animals.

TransOrGAN: An Artificial Intelligence Mapping of Rat Transcriptomic Profiles between Organs, Ages, and Sexes.

Animal studies are required for the evaluation of candidate drugs to ensure patient and volunteer safety. Toxicogenomics is often applied in these studies to gain understanding of the underlying mechanisms of toxicity, which is usually focused on critical organs such as the liver or kidney in young male rats. There is a strong ethical reason to reduce, refine and replace animal use (the 3Rs), where the mapping of data between organs, sexes and ages could reduce the cost and time of drug development. Herein, we proposed a generative adversarial network (GAN)-based framework entitled TransOrGAN that allowed the molecular mapping of gene expression profiles in different rodent organ systems and across sex and age groups. We carried out a proof-of-concept study based on rat RNA-seq data from 288 samples in 9 different organs of both sexes and 4 developmental stages. First, we demonstrated that TransOrGAN could infer transcriptomic profiles between any 2 of the 9 organs studied, yielding an average cosine similarity of 0.984 between synthetic transcriptomic profiles and their corresponding real profiles. Second, we found that TransOrGAN could infer transcriptomic profiles observed in females from males, with an average cosine similarity of 0.984. Third, we found that TransOrGAN could infer transcriptomic profiles in juvenile, adult, and aged animals from adolescent animals with an average cosine similarity of 0.981, 0.983, and 0.989, respectively. Altogether, TransOrGAN is an innovative approach to infer transcriptomic profiles between ages, sexes, and organ systems, offering the opportunity to reduce animal usage and to provide an integrated assessment of toxicity in the whole organism irrespective of sex or age.

Mitochondria and renal microvascular dysfunction following ischemia-reperfusion in rats

The pathophysiological mechanisms underlying ischemia-reperfusion (IR) induced acute kidney injury (AKI) remain poorly understood. Preglomerular microvessels (PGMV), specifically afferent arterioles, possess an intrinsic autoregulatory ability that is vital for ensuring stable renal hemodynamics. Our recent study indicates that renal autoregulation is impaired in IR rats due to reactive oxygen species (ROS) accumulation. We hypothesized that mitochondria-derived ROS (mtROS) in preglomerular microvessels contribute to renal autoregulatory impairment in IR rats. Blood-perfused juxtamedullary nephron experiments were performed on kidneys of male Sprague-Dawley rats 24 hours after IR induction (60-min, bilateral renal artery clamping). Afferent arteriolar autoregulation was assessed as perfusion pressure (PP) was increased from 65 to 170 mmHg in 15 mmHg increments. Afferent arterioles of sham-operated control rats (n=7) established pressure-mediated autoregulatory responses. Baseline diameter (100 mmHg) averaged 13.2±0.4 μm and increased to 114±4% of baseline when PP decreased from 100 to 65 mmHg. Diameter decreased to 65±3% of baseline when PP increased to 170 mmHg. In contrast, afferent arterioles from IR rats lost autoregulatory capability and remained between 90 and 100% of baseline diameter over 65-170 mmHg (n=8). Addition of Mito-Tempo (mitochondria-targeted antioxidant, 0.1 mM, n=3) to the perfusate restored autoregulation in IR rats at lower PP (65-125 mmHg, P&gt;0.05 vs sham) and partially restored it over 140-170 mmHg. Superfusion with oligomycin (ATP synthase inhibitor, 2.5 μM) in normal kidneys evoked vasodilation to 178±13% baseline and blunting of autoregulatory reactivity. Renal autoregulation is linked to ATP-sensitive P2X1-receptor signaling. Changes in ATP-induced intracellular calcium concentration ([Ca2+]i) were assessed in isolated PGMV myocytes using Fura-2 fluorescent dye. IR markedly attenuated [Ca2+]i responses to 10 and 100 μM ATP by 46±11% and 57±15%, respectively (P&lt;0.05, n=3-4 rats/group), and blunted ATP-induced afferent arteriolar vasoconstriction ( P&lt;0.05 vs. sham, n=3/group). IR markedly increased the fluorescence intensity of mitoROS (MitoSOX™ kit) in PGMV compared to sham rats. Mitochondrial respiratory function was assessed using High Resolution Respirometry in freshly isolated PGMV (n=3/group). IR significantly reduced basal respiration (20±4 vs. 58±9 pmol/s·ml in sham, P&lt;0.05) and oxidative phosphorylation capacity (51±10 vs. 219±37 pmol/s·ml in sham, P&lt;0.05). The percentage of ATP-linked respiration was also reduced in PGMV of IR (60±2% vs. 75±2% in sham, P&lt;0.05). In conclusion, mitochondria of PGMV are involved in regulating renal microvascular tone and autoregulation. IR leads to autoregulatory dysfunction by causing mitochondrial dysfunction in PGMV, increased mtROS production and suppression of ATP-dependent calcium signaling. This study is supported by grants R01DK106500. This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Preeclamptic programming unevenly perturbs inflammatory and renal vasodilatory outcomes of endotoxemia in rat offspring: modulation by losartan and pioglitazone.

Introduction: Preeclampsia (PE) enhances the vulnerability of adult offspring to serious illnesses. The current study investigated whether preeclamptic fetal programming impacts hemodynamic and renal vasodilatory disturbances in endotoxic adult offspring and whether these interactions are influenced by antenatal therapy with pioglitazone and/or losartan. Methods: PE was induced by oral administration of L-NAME (50mg/kg/day) for the last 7 days of pregnancy. Adult offspring was treated with lipopolysaccharides (LPS, 5mg/kg) followed 4-h later by hemodynamic and renovascular studies. Results: Tail-cuff measurements showed that LPS decreased systolic blood pressure (SBP) in male, but not female, offspring of PE dams. Moreover, PE or LPS reduced vasodilations elicited by acetylcholine (ACh, 0.01-7.29nmol) or N-ethylcarboxamidoadenosine (NECA, 1.6-100nmol) in perfused kidneys of male rats only. The latter effects disappeared in LPS/PE preparations, suggesting a postconditioning action for LPS against renal manifestation of PE. Likewise, elevations caused by LPS in serum creatinine and inflammatory cytokines (TNFα and IL-1β) as well as in renal protein expression of monocyte chemoattractant protein-1 (MCP-1) and AT1 receptors were attenuated by the dual PE/LPS challenge. Gestational pioglitazone or losartan reversed the attenuated ACh/NECA vasodilations in male rats but failed to modify LPS hypotension or inflammation. The combined gestational pioglitazone/losartan therapy improved ACh/NECA vasodilations and eliminated the rises in serum IL-1β and renal MCP-1 and AT1 receptor expressions. Conclusion: Preeclamptic fetal programming of endotoxic hemodynamic and renal manifestations in adult offspring depends on animal sex and specific biological activity and are reprogrammed by antenatal pioglitazone/losartan therapy.

Fermented whey modulated AFB1 and OTA-induced hepatotoxicity and nephrotoxicity in vivo. A relative and absolute quantification about sex differences

Aflatoxin B1 (AFB1) and ochratoxin A (OTA) are well-known to promote hepatotoxicity and nephrotoxicity in vivo, which may be counteracted by natural compounds like fermented whey (FW). Carbamoyl phosphate synthetase 1 (CPS1) and kidney injury molecule 1 (KIM-1) are typical biomarkers used to detect liver and kidney damage, respectively. Thus, RT-qPCR and droplet digital PCR (ddPCR) analysis were performed to assess the potential beneficial effect of FW against AFB1 and OTA hepatotoxicity and nephrotoxicity in male and female Wistar rats by analyzing the altered gene expression of hepatic CPS1 and renal KIM-1 after 28 days of oral exposure. In male livers, the most damaging treatment was AFB1 by reducing CPS1 expression, which was totally reversed by FW-administration. This bioactive compound also improved gene expression changes induced by OTA and mycotoxins mixture. In female livers, a significant CPS1 overexpression was observed for each exposure performed, in which FW-supplementation reported no remarkable differences compared with mycotoxins exposure. Conversely, in the kidneys of male and female rats, exposure to mycotoxins promoted renal damage by altering KIM-1 gene expression, being OTA-exposure the most harmful condition. In both sexes, ddPCR analysis demonstrated that FW-addition modulated mycotoxins induced KIM-1 gene expression changes, thus reducing kidney damage. In this organ, sex-related responses were not clearly observed. Therefore, these findings confirmed that AFB1 and OTA-promoted hepatotoxicity and nephrotoxicity in vivo, which could be modulated by dietary FW supplementation.

The Protective Role of Camel Milk against Reprotoxicity, Hepatotoxicity, and Nephrotoxicity in Aflatoxic-Induced Male Rats

The goal of this study was to document the toxic effects of aflatoxin B1 (AfB1) on the testis, epididymis, liver, and kidneys of adult male rats, and to employ camel milk as a natural antidote to neutralize these effects. For these purposes, 120 adult male Wister rats (90 days old) were divided into four groups (30 males each); control (C) group (drinking water was supplied), Cm group (camel milk was supplied at 10ml/kg bw/day), Af group (AfB1 was supplied at 0.3mg/kg bw/day), and CmAf group (combination treatment were supplied). The males were weighed and sacrificed on days 21 and 42 of the treatment to evaluate the histological changes of the liver, kidneys, testes, and epididymis. The body weight and testicular, epididymal, prostate, and seminal vesicle weights in the Af group decreased significantly, however this was improved in AfCm group. At day 21, histological findings of AF group revealed a decline of testicular germ layers and spermatogenesis arrest, necrotic and degenerative changes of hepatocytes and renal tubules, epididymal epithelial hyperplasia with cytoplasmic vacuolation, and depletion of sperms from the epididymis' lumen. At day 42, the severity of the histopathological changes were time-dependet. At both experimental periods, AfCm group reported substantial reduction in the degree of germ epithelium with normal seminiferous tubules epithelia with active spermatogenesis, necrosis of some hepatocytes beside infiltration of some inflammatory cells, most glomeruli and tubules were normal but some with sloughing tubular epithelia, and normal epididymalpseudostratified columnar epithelium with sperms in the lumen.

Prepubertal to adulthood exposure to low doses of glyphosate-based herbicide increases the expression of the Havcr1 (Kim1) biomarker and causes mild kidney alterations

Glyphosate is a nonselective and postemergent herbicide used to combat weeds in several crops, which raises concerns about risks to human health since residues are detected in urine, human milk, surface water and several types of food. Feces and urine are the major routes of elimination of glyphosate, making the kidney a sensitive target for the development of toxicity. In fact, farmers are at high risk of developing chronic kidney disease. In this sense, this study aims to investigate kidney function by measuring the serum levels of urea and creatinine, examining the histological morphology, and analyzing the mRNA expression of genes related to tubular transport of ions, urea and urates and the biomarker of kidney disease Kim1, and the levels of lead in the kidney in male Wistar rats orally exposed to low levels of glyphosate-based herbicide (GBH: 0, 0.5 or 5 mg/kg) from weaning to adult life by gavage. GBH0.5 showed reduced serum urea concentration, presence of tubulointerstitial swelling and mononuclear cell infiltration into the interstitium, increased gene expression of Kim1 and reduced gene expression of Slc14a1. GBH5 showed reduced serum urea and increased serum creatinine concentrations, tubulointerstitial swelling, interstitial fibrosis, and reduced expression of Trpm6 and Trpv5. Exposure to GBH did not affect the levels of Pb in the kidneys of animals. In conclusion, glyphosate at low doses may cause mild kidney damage. It is necessary to evaluate whether the long-term effects of this constant injury may contribute to the development of chronic kidney disease of uncertain etiology.

Effect of the Anticancer Drug Doxorubicin (Adriamycin) on Antioxidant Studies and Ultrastructural Investigation in the Liver, Kidney, and Heart Tissues of Male Rats

Doxorubicin is a well-known antineoplastic agent that has proved to be successful in the treatment of various types of cancer. I used rats as the model to evaluate the effect of doxorubicin on antioxidant studies and ultrastructural investigations in the liver, kidney, and heart tissues. Male albino rats were given 1.0 mg/kg body weight of the anticancer drug doxorubicin intraperitoneally three times a week for 52 days. This was for a total of 18 doses. Control animals received 52 doses of 0.5 ml of saline over 52 days. The body weights of rats injected with doxorubicin experienced a significant decrease after the last dose compared to the control group of rats. In this study, the weights of the heart, kidneys, and liver were measured. Except for cardiac tissues, the protein content in the aforementioned tissues in treated rats was significantly different from the control. Glutathione (GSH) levels in the kidneys of experimental rats were not significantly lower (7.946 ± 0.781) compared to controls (8.06 ± 0.74) but there was a non-significant increase in GSH levels in the liver (17.095 ± 1.066) compared to controls (13.8 ± 1.3). In addition, the mean GSH levels in doxorubicin-treated hearts were significantly lower (7.9462 ± 0.781) compared to controls (8.06 ± 0.74). Lipid peroxidation (Lpx) and malondialdehyde content (MDA), a marker of lipid peroxidation, were found in much lower concentrations in the liver organ of the doxorubicin-treated group (0.0162 ± 0.00086) as compared to (0.20 ± 0.02) controls, and MDA content in the kidney was decreased (0.0239 ± 0.0003) compared to control rats (0.31 ± 0.03), as well as heat production (0.0398 ± 0.00097) compared to (47.451 ± 1.708) controls. Glutathione reductase (GR) levels were significantly elevated in the same tissue treatment group. Glutathione-S-Transferase (G-S-T) activity was assessed and significantly increased in all tissues in the doxorubicin model. Glutathione peroxidase (GPx) activity showed a significant decrease in all the above tissues after doxorubicin injection. The catalase (CAT) activity of doxorubicin was greatly increased in one treated rat. In the doxorubicin-treated group, levels of cytochrome p450 (CYTp450) were significantly decreased in liver and kidney tissue and significantly elevated in heart tissue. After doxorubicin treatment, cytochrome b5 (CYTb5) levels in liver tissues increased significantly (837.177± 61.197) compared to controls (615 ± 37.0), and the contents of cytochrome b5 in rats' kidneys increased significantly (447.685 ± 35.215) compared to controls (2605.5± 259.2). and cytochrome b5 in heart tissues was lower (165.352± 8.7) when compared to controls (88± 0.4). The results showed that there were few obvious changes in histological, ultrastructural, and biochemical changes in liver tissue in the doxorubicin model. Long-term doxorubicin treatment in kidney tissue results in no significant changes at the light microscopic level, but the electron microscopic level reveals no change from a histological point of view.

Investigations into Nolvadex toxicity on the kidneys of albino male rats: Physiological and histopathological study

Introduction and Aim: Breast cancer is the most prevalent sex-based malignancy worldwide. Nolvadex is commonly used as first-line therapy for patients with breast cancer. However, studies have indicated that long-term usage of this medicine can result in nephrotoxicity, which can damage kidney tissues. So, the aim of this research was to examine what happened to the serum levels of urea, uric acid, and creatinine when the drug was given to rats in a range of different doses. Materials and Methods: Male Wistar rats (n=40) were randomly divided into four groups (n=10 each). The physiological solution (normal saline, 0.9%) was given to the control group (G1). Rats in Groups 2, 3, and 4 received Nolvadex at dosages of 30, 40, and 50 mg/kg of body weight four times weekly for a total of 10 weeks. At the end of the experimental period blood drawn from these animals were checked for serum concentrations of urea, uric acid, and creatinine. The animals were sacrificed and their kidneys subjected to histopathological examination. Data obtained was subjected to statistical analysis. Results: The levels of urea, uric acid, and creatinine that were discovered in the experimental groups were all determined to be significantly higher than the levels that were discovered in the control group. In the experimental group that was given Nolvadex, an infiltration of inflammatory cells, blood congestion, pyknic and necrotic nuclei in the glomerulus, substantial epithelial deterioration in the renal tubules, and an altered renal tissue architecture were detected. Conclusion: Serum levels of urea, uric acid and creatinine levels increased when experimental rats were administered with varying concentration of the drug Nolvadex. Its administration caused alteration to the architecture of renal tissue.

Effect of oral administration of Fadogia cienkowskii Shweinf. (Rubiaceae) ethanol root extract on some semen parameters, testes, epididymis, liver and kidney of male albino rats

The use of medicinal plants to enhance sexual performance and satisfaction is practiced in many regions of the world. Many of these plants are used with little or no scientific information about their effects on the body including effect on vital sex organs like testes and epididymis. Fadogia cienkowskii is a flowering plant whose roots are used in some communities in Africa for the management of sexual dysfunction and infertility. There is paucity of information however, on its effect on semen quality, gonads, liver and kidney after oral administration, thus the need for this study. Four groups of male albino rats were orally administered with 0, 50, 100 and 200 mg/Kg body weight of Fadogia cienkowskii ethanol root extract for 40 days. The rats were humanely euthanized on the 41st day. Blood was collected and processed for serum biochemical analysis, while samples of tissues from the testis, epididymis, liver and kidney were processed for histo-pathological examination. Semen was retrieved from the caudal epididymis and used to determine some semen quality parameters. At 200 mg/kg, the extract significantly increased sperm count and the testes and epididymis histo-architecture did not show any pathology. The serum biochemical parameters of liver and kidney function showed no pathologic alterations; however, the liver and kidney histology showed various degrees of pathological lesions. It was concluded that 70% ethanol root extract of Fadogia cienkowskii increased sperm count at 200 mg/kg dose, not toxic to the testes and epididymis but suggestive of liver and kidney toxicity.

Ameliorative Effect of Rice Husk Methanol Extract on Liver and Kidney Toxicities Induced by Subchronic Codeine Administration.

Background and Objective. Rice husk remains a key by-product of rice milling generated in significant amount. Accumulated evidence indicates that rice husk contains numerous bioactive compounds; however, its application is limited. This study was designed to introduce an in vivo application of rice husk extract, against opioid-induced liver and kidney injuries. Codeine was considered a psychotic inducer in this study due to its global alarming misuse recently. The hepatorenal ameliorative proclivity of rice husk extract against codeine-induced toxicity on the liver and kidney in male albino Wistar rats was examined. To this effect, thirty-six (36) albino Wistar rats of weight 100-110 g were utilized and weight-matched animals placed in 6 groups of 6 rats each. After 30 days of the combined administration of codeine and the rice husk extract, the experimental animals were assayed for basic liver and renal markers such as AST, ALP, ALT, total protein, albumin, conjugated and total bilirubin, urea, creatinine, and electrolytes (sodium, potassium, chloride, and bicarbonate). Rice husks were collected from a local rice mill, and the extraction was done with methanol. Findings. Rice husk extract (RHE) significantly ameliorated the recorded hepatic damage. More so, the extract showed a significant action on the renal markers as well. A histopathology examination of the liver and kidney tissues revealed that RHE showed a hepatorenal ameliorative potential in a dose-dependent manner. Conclusion. Phytonutrient from RH possesses a healing ability against opioid-induced hepatorenal toxicity. Thus, RH is safe for human and may be adopted to obviate and manage codeine-induced hepatorenal damage or injury. Significance and Novelty. Data on the application of RHE as a phytonutrient to combat liver and kidney injuries were demonstrated. Future studies should evaluate its potential on other organs.

Rhizophora apiculata Bark Ethanolic Extracts Prevent Kidney Damage Caused by Cigarette Smoke in Male Rats

Rhizophora apiculata mangrove bark contains high levels of antioxidants, including triterpenoids, steroids, saponins, and tannins. The high antioxidant content can prevent oxidative stress, one of which is caused by free radicals from cigarette smoke. This research aimed to determine the potential of Rhizophora apiculata mangrove bark to protect against damage to the kidney organs of male white rats (Rattus novergicus) of the Sprague-Dawley strain exposed to cigarette smoke. This study used 25 mice divided into 5 groups for 30 days, namely group K(-), which was not given exposure to cigarette smoke and mangrove bark extract; group K(+), which was only given exposure to cigarette smoke; group P1, which was given the extract mangrove bark with a dose of 26.27 mg/kg BW and given exposure to cigarette smoke 24 cigarettes per day, group P2 which was given mangrove bark extract with a dose of 56.55 mg/kg BW and given exposure to cigarette smoke 24 cigarettes per day, and group P3 which was given mangrove oil bark extract at a dose of 113.1 mg/kg BW and given exposure to cigarette smoke 24 cigarettes per day. On day 31, the rats were euthanized, and their kidneys were prepared for histology. Kidney histology was observed, and kidney damage was assessed from the histology of glomerular and renal tubular damage. The kidney damage score is 0 if there was no damage, 1 if inflammatory cell infiltration was found, 2 if Bowman space edema or swelling of tubular epithelial cells was found, 3 if necrosis was found. Then, take the average of each renal tubular and glomerular damage score and add them together for a total damage score, namely 0-6. The median kidney damage score in the K (-) group was 0.4, the K (+) group was 3.6, the P1 group was 2.4, the P2 group was 2.4, and the P3 group was 2.2. The results of the Kruskal-Wallis test obtained a p-value of 0.001, meaning there were significant differences in at least the two treatment groups. This research showed that administering Rhizophora apiculata mangrove bark extract could prevent histological damage to the kidneys of male white rats of the Sprague-Dawley strain caused by cigarette smoke.

Morphological, immunohistochemical, and biochemical study on the ameliorative effect of gallic acid against bisphenol A-induced nephrotoxicity in male albino rats

This study aimed to determine the effect of gallic acid (GA) on ameliorating bisphenol A (BPA) nephrotoxicity in male rat kidneys. Forty rats were assigned randomly into two groups: control (ten animals) and BPA (40 mg/kg bwt) (thirty animals), the second group was divided into three subgroups: BPA alone, BPA + G50 (50 mg/kg bwt), and BPA + G200 (200 mg/kg bwt). The biochemical analysis included measurements of the contents of nitric oxide, lipid peroxidation, reactive oxygen species, and cytokines (interleukin-1α and interleukin-6) in the kidney. The antioxidant enzymes catalase and superoxide dismutase were also measured in the kidney. Kidney function was assessed by determining uric acid, urea, and creatinine levels. The morphological investigations included hematoxylin and eosin staining for assessing the general histology and determining the glomerular and corpuscular areas, the tubular cell degeneration mean area, and the mean leukocyte infiltration area. Also, collagen fiber intensity and polysaccharide content were analyzed. Furthermore, immunohistochemical, morphometric, and ultrastructural studies were carried out. The results revealed morphological, immunohistochemical, and biochemical alterations in the kidney. Most of these changes showed a satisfactory improvement of kidney damage when BPA-administered rats were treated with GA at both doses. In conclusion, GA exhibited a strong protective effect against BPA-induced nephrotoxicity.

Effect of aqueous extract Lawsonia inermis leaves on Urea, Creatinine and Histological of kidneys in white male Rats exposed to oxidative stress of H2O2

This study was designed to examine, the effect of Effective aqueous extract Lawsonia inermis leaves as antioxidant on concentration of Urea ,Criatinine and Histological of kidneys in Albino male Rats exposed to hydrogen peroxide induced oxidative stress. This study showed that 0.5% hydrogen peroxide concentration leds to significant increase (P&lt;0.05( in concentration of serum urea and creatinine comparing with control group. While the aqueous extract of Lawsonia inermis concentration (50mg/kg) led to significant decrease (P&lt;0.05) in concentration of serum urea and creatinine compare with control group. Also the results showed no significant increase in concentration of urea and creatinine in group exposed to oxidative stress and aqueous extract of Henna comparing with control group. The histological results of the kidney treated with (0.5%) H2o2 showed degeneration, congestion, lymphatic infilteration, vacuolation in the renal tubules with necrosis comparing with control. While sections of kidney treated with aqueous extract of Henna showed normal appearance of the renal tubules. Histological investigation of kidneys rats treated with H2O2 and extract of Henna showed improvement in histological picture with reduction in infilteration, vacuolation and necrosis but the tissue did not return back to the normal state.

Depleted uranium causes renal mitochondrial dysfunction through the ETHE1/Nrf2 pathway

The kidney is the main organ affected by acute depleted uranium (DU) toxicity. The mechanism of nephrotoxicity induced by DU is complex and needs to be further explored. This study aimed to elucidate the function of mitochondrial dysfunction in nephrotoxicity generated by DU and confirm the latent mechanism. We verified that DU (2.5–10 mg/kg) caused mitochondrial dysfunction in male rat kidneys and decreased ATP content and the mitochondrial membrane potential. In addition, melatonin (20 mg/kg), as an antioxidant, alleviated DU-induced oxidative stress and mitochondrial dysfunction in male rats, further reducing kidney damage caused by DU. These results indicate that mitochondrial dysfunction plays a vital role in DU nephrotoxicity. When ethylmalonic encephalopathy 1 (ETHE1) was knocked down, DU-induced oxidative stress and mitochondrial dysfunction were increased, and renal injury was aggravated. When exogenous ETHE1 protein was applied to renal cells, the opposite changes were observed. We also found that ETHE1 knockdown increased the expression of NF-E2-related factor 2 (Nrf2), a vital oxidative stress regulator, and its downstream molecules heme oxygenase-1 (HO-1) and NADPH quinone oxidoreductase 1 (NQO1). Nrf2 knockout also aggravated DU-induced oxidative stress, mitochondrial dysfunction, and kidney damage. In conclusion, DU causes oxidative stress and antioxidant defense imbalance in renal cells through the ETHE1/Nrf2 pathway, further causing mitochondrial dysfunction and ultimately leading to nephrotoxicity.

Effects of Psychoactive Substances on Some Biochemical Parameters and Histopathology of Kidney in Male Albino Rats

Effects of Psychoactive Substances on Some Biochemical Parameters and Histopathology of Kidney in Male Albino Rats