Effect of thiram on rat kidney: inhibition of brush border membrane and antioxidant enzymes, diminution of antioxidant capacity, enhanced DNA damage and DNA-protein cross-linking

2021 ◽  
Author(s):  
Samreen Salam ◽  
Amin Arif ◽  
Aijaz Ahmed Khan ◽  
Riaz Mahmood
Keyword(s):  
Antioxidant Enzymes ◽  
Antioxidant Capacity ◽  
Brush Border ◽  
Brush Border Membrane ◽  
Male Rats ◽  
Cross Linking ◽  
Control Group ◽  
Human Beings ◽  
Glutamyl Transferase ◽  
Protein Cross Linking

Abstract Thiram is a dithiocarbamate pesticide that is widely used as a fungicide to protect crops and seeds, especially in China and India. Although thiram is considered relatively safe for humans but due to its persistent nature it may become a health hazard for human beings and animal if long term exposure takes place. The aim of the present work was to study the effects of oral administration of thiram on kidney of male rats given different doses of thiram (100, 250, 500, 750 mg/kg body weight) for 4 consecutive days. This treatment significantly reduced cellular glutathione and total sulfhydryl content but enhanced protein carbonyl and hydrogen peroxide levels. The plasma creatinine and BUN levels were also elevated indicating nephrotoxicity. The activities of antioxidant enzymes catalase, superoxide dismutase, glutathione peroxidase, thioredoxin reductase and glutathione-S-transferase were significantly decreased. The antioxidant capacity was diminished resulting in less free radical quenching and metal reducing ability of kidney. Administration of thiram also led to inhibition of intestinal brush border membrane enzymes: alkaline phosphatase, leucine aminopeptidase, γ-glutamyl transferase and maltase. Activities of enzymes of glucose metabolism viz. glycolysis, citric acid cycle, pentose phosphate pathway and gluconeogenesis were also inhibited. Histopathology of kidney tissue revealed tubular dilation, tubular cast, breaking of apical cytoplasm and intestinal hemorrhage. A significant increase in DNA fragmentation, DNA strand breaks and DNA-protein cross-linking was also observed in thiram treated rats compare to control group. These changes in kidney could be due to marked perturbation in antioxidant defense system induced by free radicals generated upon exposure to thiram.

scholarly journals The protective role of CsNPs and CurNPs against DNA damage, oxidative stress, and histopathological and immunohistochemical alterations induced by hydroxyapatite nanoparticles in male rat kidney

2019 ◽  
Vol 8 (5) ◽  
pp. 741-753 ◽  
Author(s):  
Israa F. Mosa ◽  
Mokhtar I. Yousef ◽  
Maher Kamel ◽  
Osama F. Mosa ◽  
Yasser Helmy
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Enzymes ◽  
Biological Effects ◽  
Male Rats ◽  
Nuclear Antigen ◽  
Male Rat ◽  
Control Group ◽  
Renal Tubules ◽  
Hydroxyapatite Nanoparticles

Abstract Hydroxyapatite nanoparticles (HAP-NPs) are an inorganic component of natural bone and are mainly used in the tissue engineering field due to their bioactivity, osteoconductivity, biocompatibility, non-inflammatory, and non-toxicity properties. However, the current toxicity data for HAP-NPs regarding human health are limited, and only a few results from basic studies have been published. Therefore, the present study was designed to investigate the beneficial role of chitosan nanoparticles (CsNPs) and curcumin nanoparticles (CurNPs) in alleviating nephrotoxicity induced by HAP-NPs in male rats. The results showed that HAP-NPs caused a reduction in antioxidant enzymes and induced lipid peroxidation, nitric oxide production and DNA oxidation. Moreover, HAP-NP administration was associated with intense histologic changes in kidney architecture and immunoreactivity to proliferating cell nuclear antigen (PCNA). However, the presence of CsNPs and/or CurNPs along with HAP-NPs reduced the levels of oxidative stress through improving the activities of antioxidant enzymes. Also, the rats administered the nanoparticles showed a moderate improvement in glomerular damage which matched that of the control group and showed mild positive reactions to PCNA–ir in glomeruli and renal tubules in the cortical and medullary portions. These novel insights confirm that the presence of chitosan and curcumin in nanoforms has powerful biological effects with enhanced bioactivity and bioavailability phenomena compared to their microphase counterparts. Also, they were able to ameliorate the nephrotoxicity induced by HAP-NPs.

scholarly journals PROTECTIVE ROLE AND ANTIOXIDANT ACTIVITY OF AQUEOUS EXTRACT OF ROSMARINUS OFFICINALIS AGAINST TRICHLOROACETATE-INDUCED TOXICITY IN LIVER OF MALE RATS

2018 ◽  
Vol 11 (6) ◽  
pp. 420
Author(s):  
Medhat Mostafa Abozid ◽  
Hoda Ea Farid
Keyword(s):  
Aqueous Extract ◽  
Liver Damage ◽  
Protective Role ◽  
Rosmarinus Officinalis ◽  
Male Rats ◽  
Control Group ◽  
Albino Rats ◽  
Gamma Glutamyl Transferase ◽  
Group I ◽  
Glutamyl Transferase

 Objective: The current study was designed to estimate the potential protective role of the aqueous extract of rosemary (AER) (Rosmarinus officinalis) against trichloroacetic acid (TCA)-created hepatotoxicity in male albino rats.Methods: Forty male albino rats were separated into four groups of ten: Group I served as control; Group II was given AER (200 mg/kg/day) by gavage; Group III received TCA at the dose 50 mg/kg/day, and Group V was treated with AER (200 mg/kg/day) and received TCA (50 mg/kg/day). The experiment was carried out for 2 months.Results: The toxicity of TCA for rats was revealed by an elevation in liver marker enzymes activities (gamma-glutamyl transferase [GGT], alkaline phosphatase [ALP], aspartate transaminase [AST], alanine aminotransferase [ALT]) and conjugated bilirubin (CB) level, and a decrease in albumin and total protein (TP) levels. The TCA administration also caused a significant increase in the activities of catalase (CAT), glutathione peroxidase (GPx) and superoxide dismutase (SOD), and also malondialdehyde (MDA) level in liver tissues. These biochemical effects were accompanied by histological indicators of liver damage. Treatment with ARE recovered the liver damage instigated by TCA, as showed by perfection of liver enzyme markers (GGT, ALT, AST, ALP), CB, TP and albumin; as well as antioxidant parameters (CAT, SOD, GPx) and lipid peroxidation (MDA) and amelioration of histopathology changes in the liver tissues.Conclusion: It could be concluded that AER supplementation for 2 months in TCA-induced toxicity in rats benefited hepatic antioxidant status and improved liver injury and damage in male albino rats exposed to TCA.

scholarly journals Roles of Moringa oleifera Leaf Extract in Improving the Impact of High Dietary Intake of Monosodium Glutamate-Induced Liver Toxicity, Oxidative Stress, Genotoxicity, DNA Damage, and PCNA Alterations in Male Rats

2018 ◽  
Vol 2018 ◽  
pp. 1-11 ◽  
Author(s):  
Tarfa Albrahim ◽  
Manal Abdulaziz Binobead
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Leaf Extract ◽  
Liver Toxicity ◽  
Monosodium Glutamate ◽  
Male Rats ◽  
Control Group ◽  
Gamma Glutamyl Transferase ◽  
Glutamyl Transferase ◽  
The Impact

It is common for food to be made more palatable through the use of the flavour enhancer monosodium glutamate, also known as vetsin powder. The purpose of the study described in this paper was to explore how vetsin-induced hepatic toxicity, DNA fragmentation, damage, and oxidative stress modifications could be mitigated with moringa leaf extract (MLE). To that end, 40 male rats were separated into four groups: normal control, positive control or MLE, vetsin, and vetsin combined with MLE. Results indicated that, compared to the control group, the levels of serum alanine aminotransferase (ALT), aminotransferase (AST), alkaline phosphatase (ALP), gamma-glutamyl transferase (GGT), liver malondialdehyde (MDA), DNA damage, injury, PCNA, and P53 expressions were significantly enhanced by the administration of vetsin (P<0.05). However, the vetsin group had significantly reduced levels of albumin, globulin, total protein, liver glutathione (GSH), superoxide dismutase enzyme (SOD), catalase, and glutathione S-transferase (GST) enzyme activities (P<0.05) by comparison to control. Meanwhile, modifications in liver functions, oxidative stress, DNA damage, liver injury, and PCNA expression were alleviated when vetsin was administered alongside MLE. The authors conclude that vetsin may have many side effects and that MLE can ameliorate biochemical changes, oxidative stress, hepatic injury, PCNA, and P53 alterations induced by vetsin administration.

scholarly journals The possibilities of pharmacological correction of ademol oxidative stress in rates with traumatic brain injury

2021 ◽  
Vol 25 (2) ◽  
pp. 192-195
Author(s):  
S. I. Semenenko
Keyword(s):  
Oxidative Stress ◽  
Traumatic Brain Injury ◽  
Lipid Peroxidation ◽  
Antioxidant Enzymes ◽  
Brain Injury ◽  
Oxidative Degradation ◽  
Male Rats ◽  
Control Group ◽  
Nacl Solution ◽  
Amantadine Sulfate

Annotation. An important measure of intensive care in patients with traumatic brain injury (TBI) is the use of pharmacotherapeutic agents with antioxidant properties. The aim of this study was to evaluate the effect of ademol compared with amantadine sulfate and 0.9% NaCl solution on the course of oxidative stress in the brain of TBI rats. The experiments were performed on 28 white male rats weighing 160-190 g. The experimental TBI model of severe severity was caused by the action of a carbon dioxide flow under pressure created using a gas balloon pneumatic gun. The therapeutic effect of ademol on model TBI was evaluated with a 2 mg/kg dose. The pseudoperated animals and control group received a 0.9% solution of NaCl and amantadine sulfate at a dose of 2 ml/kg and 5 mg/kg i/v. Data were processed using StatPlus 2009. We used the parametric criterion of t-Student, non-parametric criterion of W. White, paired criterion Ť. Wilcoxon, Fisher's angular transformation at p <0,05. In the course of the experiment, it was found that treatment of rats with TBI ademol leads to a decrease in the activity of lipid peroxidation and oxidative degradation of proteins (p<0.05) and promotes the normalization of the activity of antioxidant enzymes in cells of traumatically damaged brain (p<0.05). The use of ademol compared to amantadine sulfate and 0.9% NaCl solution was accompanied by a more significant decrease in the activity of lipid peroxidation and oxidative degradation of proteins and an improvement in the level of antioxidant enzymes in damaged brain of animals with TBI (p<0.05).

Thyroid hormone stimulates the Na(+)-PO4 symporter but not the Na(+)-SO4 symporter in renal brush border

1993 ◽  
Vol 265 (2) ◽  
pp. F323-F326 ◽  
Author(s):  
K. W. Beers ◽  
T. P. Dousa
Keyword(s):  
Thyroid Hormone ◽  
Thyroid Hormones ◽  
Adult Male ◽  
Brush Border ◽  
Brush Border Membrane ◽  
Male Rats ◽  
Similar Degree ◽  
Renal Brush Border Membrane ◽  
High Phosphate ◽  
Renal Brush Border

In our previous studies we established that thyroid hormones [L-thyroxine (T4) or 3,5,3'-triiodothyronine (T3)] elicit an increase in Na(+)-Pi symport in rat and mouse renal brush-border membrane (BBM) vesicles (BBMV), but the Na(+)-coupled symports of other solutes were not influenced. However, a recent report [H. S. Tenenhouse, J. Lee, and N. Harvey. Am. J. Physiol. 261 (Renal Fluid Electrolyte Physiol. 30): F420-F426, 1991]claimed that T3 increases to a similar degree both Na(+)-Pi symport and Na(+)-SO4 symport in murine renal BBM. Adult male rats were fed either normal (0.7% Pi; NPD) or high-phosphate (1.4% Pi; HPD) diet and received T3 (0.2 mg/100 g body wt ip) for 3 days before the kidneys were removed, BBMV were prepared, and the transport rates were determined. Although the Na(+)-Pi symport significantly increased (delta = +35%) in both NPD and HPD rats treated with T3, the Na(+)-35SO4 symport and Na(+)-D-[3H]glucose symports were not influenced by T3. Furthermore, treatment of NPD-fed mice with T3 using a similar protocol as rats resulted in a significant increase (delta = +26%) of Na(+)-(Pi)4 symport, but did not alter Na(+)-SO4 symport or Na(+)-glucose symport. Our findings thus document that T3 regulates selectively the Na(+)-Pi symporter in BBM without having any effect on other major divalent anions, such as SO4.

Chronic Addiction to Tramadol and Withdrawal Effect on the Spermatogenesis and Testicular Tissues in Adult Male Albino Rats

Pharmacology ◽  
2019 ◽  
Vol 103 (3-4) ◽  
pp. 202-211 ◽  
Author(s):  
Marwan Abdel-Latif Ibrahim ◽  
Alaa-Eldin Salah-Eldin
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Enzymes ◽  
Adult Male ◽  
Rna Extraction ◽  
B Cell Lymphoma ◽  
Experimental Period ◽  
Male Rats ◽  
Control Group ◽  
Albino Rats ◽  
Withdrawal Effect

Aim: The present study aimed to elucidate the effects of tramadol on the testicular functions of adult male rats due to the chronic usage of tramadol and the effect of its withdrawal. Method: Adult male albino rats were classified into the following 3 groups: (I) a control administered with normal saline and (II) tramadol-treated rats (40 mg/kg b.w. orally) for 21 successive days; and (III) like the rats in the second group but kept for 4 weeks after the last tramadol dose to study the effect of tramadol withdrawal. At the end of the experimental period, blood was collected and specimens from testis were taken for histopathological, biochemical, and molecular studies. A reverse transcription-polymerized chain reaction after RNA extraction from specimens was detected for the anti-apoptotic and pro-apoptotic genes in testicular tissues. Also, malondialdehyde (MDA) was measured in tissues homogenate and antioxidant enzymes activities were evaluated. Results: The results of this study demonstrated histological changes in testicular tissues in groups II and III compared to the control group, accompanied with increased apoptotic index and proved by increased B-cell lymphoma-2 (Bcl-2) associated-X-protein and caspase-3 expression, whereas anti-apoptotic Bcl-2 markedly decreased. Moreover, in tramadol-abused and -withdrawal groups, the MDA level increased, while the antioxidant enzymes activity decreased and revealed oxidative stress, indicating that tramadol is harmful at the cellular level and can induce apoptotic changes in testicular tissues. The withdrawal effect showed signs of improvement, but it did not return to normal levels. Conclusions: It could be concluded that the administration of tramadol causes abnormalities on testicular tissues associated with oxidative stress, which confirmed the risk of increased oxidative stress on testicular tissues due to tramadol abuse.

scholarly journals Na+/glucose co-transporter abundance and activity in the small intestine of lambs: enhancement by abomasal infusion of casein

2003 ◽  
Vol 89 (5) ◽  
pp. 573-580 ◽  
Author(s):  
Sameer J. Mabjeesh ◽  
Dafna Guy ◽  
David Sklan
Keyword(s):  
Small Intestine ◽  
Glucose Uptake ◽  
Brush Border ◽  
Brush Border Membrane ◽  
Membrane Vesicles ◽  
Control Group ◽  
Abomasal Infusion ◽  
Group A ◽  
Small Intestinal ◽  
Infusion Period

The purpose of the present study was to determine the effect of abomasal casein infusion on glucose uptake and abundance of the Na+/glucose co-transporter (SGLT1) 1 in the ovine small intestine. Lambs (body weight 35 (SEM 1·0) kg) were surgically fitted with abomasal infusion catheters and were fed diets containing equal portions of wheat hay and cracked maize. Lambs were infused with either 500 g water/d or with 500 g water containing 35 g casein/d. The infusion period lasted 10 d, after which lambs were killed, exsanguinated and eviscerated. Brush border membrane vesicles (BBMV) were prepared using mucosa from different small intestinal regions. Intake and total tract digestibility of nutrients were similar between treatments and averaged 1134, 1142 and 486 g/d and 67, 70, and 94 % for DM, organic matter and non-structural carbohydrates respectively. Crude protein (N×6·25) digestibility was 15 % greater in the casein-infused than control lambs. Glucose uptake to BBMV ranged from 101 to 337 pmol/mg protein per s along the small intestine and was greatest in the mid-section of the small intestine. In the mid-jejunum, glucose uptake was greater (P<0·07) in lambs infused with casein and averaged 120 pmol/mg protein per s compared with 68 pmol/mg protein per s in the control group. SGLT1 affinity was similar between treatments and averaged 104 μM in the different segments of the small intestine of lambs. However, lambs infused with casein exhibited similar values along the small intestine and affinity averaged 106 μm, while in the control group a greater affinity (85 μm) was measured in the mid-jejunum. SGLT1 protein abundance was correlated with glucose uptake in the BBMV in the casein-treated lambs, but not in the control group. These results suggest that glucose uptake along the small intestine of lambs is influenced by casein or its derivatives in the small intestine via SGLT1 affinity and activity at the brush border membrane, and that SGLT1 activity may be regulated by post-translational events affected by amino acids and peptides.

Neuroprotective Effect of Nilotinib on Cortical Pyramidal Cells, Histological, Morphometric and Biochemical Study

2020 ◽  
pp. 23-33
Author(s):  
Ahmed S. Ahmed
Keyword(s):  
Cell Death ◽  
Antioxidant Enzymes ◽  
Antiepileptic Drug ◽  
Neuroprotective Effect ◽  
Latency Period ◽  
Neuronal Cell ◽  
Pyramidal Cells ◽  
Male Rats ◽  
Control Group ◽  
Cortical Tissue

Introduction: Death of neuronal cell and gliosis are the two main pathological hallmarks induced by nervous tissue stress like conditions such as status epilepticus. Previous studies have mentioned that neuronal cell death occur as a result of different mechanisms, namely, necrosis and apoptosis. Although more recent studies have explained the cell death on the basis of autophagy. Many antiepileptic drugs are marketed, taking into consideration the antioxidant role of nilotinib and support its use as a favorable antiepileptic drug. The aim of the present study is to assess the neuroprotective effect of antiepileptic drug nilotinib on cortical tissue in rats. Materials and Methods: Sixty adult male rats were divided into three groups: (1) Control group, (2) pentylenetetrazol group (injected with pentylenetetrazol 60 mg/kg, subcutaneously), (3) nilotinib and pentylenetetrazol group (pretreated with nilotinib, 25 mg/kg daily for seven days prior to pentylenetetrazol administration). Latency of seizure and level of either oxidant or antioxidant enzymes in the cortical tissue was assessed. The histopathological changes in the cerebral cortex were studied also using hematoxylin and eosin stain. Results: Nilotinib increased the latency period of convulsions, increased the antioxidant enzymes levels with regain of the normal histological features. Conclusions: Nilotinib proved to promote the antioxidant, antiapoptotic pathways, anti-inflammatory and inhibiting autophagy which favor its use as an anti-epileptic drug.

scholarly journals Long-Term Adverse Effects of Oxidative Stress on Rat Epididymis and Spermatozoa

Antioxidants ◽  
2020 ◽  
Vol 9 (2) ◽  
pp. 170 ◽  
Author(s):  
Pei You Wu ◽  
Eleonora Scarlata ◽  
Cristian O’Flaherty
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Antioxidant Enzymes ◽  
Sperm Quality ◽  
Dna Oxidation ◽  
Male Rats ◽  
Saline Control ◽  
Control Group ◽  
Long Term Effects

Oxidative stress is a common culprit of several conditions associated with male fertility. High levels of reactive oxygen species (ROS) promote impairment of sperm quality mainly by decreasing motility and increasing the levels of DNA oxidation. Oxidative stress is a common feature of environmental pollutants, chemotherapy and other chemicals, smoke, toxins, radiation, and diseases that can have negative effects on fertility. Peroxiredoxins (PRDXs) are antioxidant enzymes associated with the protection of mammalian spermatozoa against oxidative stress and the regulation of sperm viability and capacitation. In the present study, we aimed to determine the long-term effects of oxidative stress in the testis, epididymis and spermatozoa using the rat model. Adult male rats were treated with tert-butyl hydroperoxide (t-BHP) or saline (control group), and reproductive organs and spermatozoa were collected at 3, 6, and 9 weeks after the end of treatment. We determined sperm DNA oxidation and motility, and levels of lipid peroxidation and protein expression of antioxidant enzymes in epididymis and testis. We observed that cauda epididymal spermatozoa displayed low motility and high DNA oxidation levels at all times. Lipid peroxidation was higher in caput and cauda epididymis of treated rats at 3 and 6 weeks but was similar to control levels at 9 weeks. PRDX6 was upregulated in the epididymis due to t-BHP; PRDX1 and catalase, although not significant, followed similar trend of increase. Testis of treated rats did not show signs of oxidative stress nor upregulation of antioxidant enzymes. We concluded that t-BHP-dependent oxidative stress promoted long-term changes in the epididymis and maturing spermatozoa that result in the impairment of sperm quality.

Preventive Effect of Carvacrol Against Oxidative Damage in Aged Rat Liver

2017 ◽  
Vol 87 (1-2) ◽  
pp. 59-65 ◽  
Author(s):  
Saeed Samarghandian ◽  
Mohsen Azimi-Nezhad ◽  
Tahereh Farkhondeh
Keyword(s):  
Lipid Peroxidation ◽  
Antioxidant Enzymes ◽  
Matched Control ◽  
Male Rats ◽  
Antioxidant Defenses ◽  
Control Group ◽  
Aged Rats ◽  
Preventive Effect ◽  
Glutathione S Transferase ◽  
Old Rats

Abstract. The present study was designed to investigate the changes in activities of antioxidant enzymes and lipid peroxidation level in the liver of 2, 10 and 20 months old rats, and to see whether these changes are restored to those of the two month old rats after carvacrol treatment. Male rats of 2, 10, and 20 months (n = 10 for each group) were used for all the experiments. The aged rats (10 and 20 months old) were given carvacrol (15 mg/day per body weight) for 30 days. Control animals received an equal volume of vehicle. After the treatment, livers were removed for estimation of superoxide dismutase-SOD, glutathione-S-transferase-GST, catalase-CAT activities and lipid peroxidation level. The present findings determined that normal aging was associated with a significant decrease in the activities of antioxidant enzymes (SOD; 11.87 ± 0.6 (2 months old) vs 7.56 ± 0.1 (20 months old); P < 0.001) in liver, as well as an increase in lipid peroxidation level (MDA; 0.15 ± 0.01 (2 months old) vs 0.41 ± 0.01 (20 months old); P < 0.001) in aged rats. Also, the results of this study indicated that carvacrol treatment increased the activities of the antioxidant enzymes in 20 months old animals versus the aged matched control group (SOD; 9.87 ± 0.4; P < 0.01). Furthermore, carvacrol decreased lipid peroxidation content in 10 and 20 months old animals compared with the aged matched control (MDA; 9.87 ± 0.4; P < 0.001). Our data shows that carvacrol could be a candidate to inhibit the development of age-induced liver damage through inhibition of oxidative stress and also increasing antioxidant defenses.

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