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Dataset on biochemical markers and histological alterations in rat kidney intoxicated with cadmium chloride and treated with antioxidant

This dataset demonstrates the in vivo renal histology and biochemical activity of Atorvastatin (AT) in cadmium-induced nephrotoxic rat model. Fifty-six adult male Wistar rats assigned to eight groups. Rats were treated with physiologic saline at a volume of 4 mg/kg, contained Atorvastatin at a dose of 20 mg/kg body weight for 15 days. The intraperitoneal administration of cadmium chloride at doses of 1, 2, 1 and 3 mg/kg started on day 8. On day 16, samples were collected for biochemical and histological analyses. Data of renal function were estimated in the serum and organ. Cadmium chloride increased malondialdehyde (MDA), blood urea nitrogen (BUN), and creatinine (Cr) serum level and decreased superoxide dismutase (SOD), glutathione peroxidase (GPx) and glutathione (GSH) levels. Administration of Atorvastatin significantly increased lipid peroxidation and renal decreased glutathione and antioxidant enzymes activity and significantly decreased BUN and Creatinine levels. Data were supported by histological examination indicated improved changes and kidney protective potential following cadmium chloride-induced oxidative stress.


a b s t r a c t
This dataset demonstrates the in vivo renal histology and biochemical activity of Atorvastatin (AT) in cadmium-induced nephrotoxic rat model. Fifty-six adult male Wistar rats assigned to eight groups. Rats were treated with physiologic saline at a volume of 4 mg/kg, contained Atorvastatin at a dose of 20 mg/kg body weight for 15 days. The intraperitoneal administration of cadmium chloride at doses of 1, 2, 1 and 3 mg/kg started on day 8. On day 16, samples were collected for biochemical and histological analyses. Data of renal function were estimated in the serum and organ. Cadmium chloride increased malondialdehyde (MDA), blood urea nitrogen (BUN), and creatinine (Cr) serum level and decreased superoxide dismutase (SOD), glutathione peroxidase (GPx) and glutathione (GSH) levels. Administration of Atorvastatin significantly increased lipid peroxidation and renal decreased glutathione and antioxidant enzymes activity and significantly decreased BUN and Creatinine levels. Data were supported by histological examination indicated improved changes and kidney protective potential following cadmium chloride-induced oxidative stress.

Value of the Data
• The dataset presents favourable evidence concerning the effect of Atorvastatin treatment on oxidative stress biomarkers (MDA, SOD, GPx, and GSH) and histological structure data in cadmium chloride-induced nephrotoxicity in Wistar rat model. • The antioxidant activity data of Atorvastatin at the dose of 20 mg/kg body weight in rats intoxicated with cadmium chloride provides researchers with reference for further experimental studies • The data supported Atorvastatin protective effect in cadmium-induced kidney intoxication in rat model and therefore, may be used for further experiments in investigating the potential Atorvastatin preventive effect against kidney damage in workers who are occupationally exposed to Cadmium.
• These data indicate Atorvastatin improves lipid peroxidation, BUN, and Creatinine serum levels and reduces adverse histological changes in rat kidney tissues induced by cadmium chloride. • The insights gained from these data may allow researchers explain the role of Atorvastatin treatment on the cadmium chloride-induced oxidative stress in rat nephrotoxicity.

Data description
The current data article describes the effect of Atorvastatin treatment on oxidative stress biochemical markers and histological changes in rat nephrotoxicity induced by cadmium chloride. Fig. 1 presents the experimental steps that were conducted to collect data on biochemical and histological parameters.      and CdCl2 at a dosage of 1 mg/kg body weight ( Fig. 6 ). Group 5 treated with CdCl2 at a dosage of 2 mg/kg body weight ( Fig. 7 ). Group 6 treated with Atorvastatin at a dosage of 20 mg/kg body weight and CdCl2 at a dosage of 2 mg/kg body weight ( Fig. 8 ). Group 7 treated with CdCl2 at a dosage of 3 mg/kg body weight ( Fig. 9 ). Group 8: treated with Atorvastatin at a dosage of 20mg/kg body weight and CdCl2 at a dosage of 3 mg/kg body weight ( Fig 10 ).
Light micrographs of kidney sections of rats following treatment periods with normal saline, cadmium chloride, and pretreatment with Atorvastatin are shown in Fig. 11 , Fig. 12 , and Fig. 13 respectively. Histopathological analysis of the renal tissues focused on changes in glomeruli, Cortex and medullary segments.
Detailed data on the Tukey's comparisons of biochemical parameters (BUN, creatinine, GSH, MDA, SOD, and GPx) in the treatment groups of cadmium chloride-induced nephrotoxic rats  with or without saline and Atorvastatin treatments are presented in the Excel data file 1 available at Mendeley repository mentioned in the above specifications table.
Results of raw data on the measurements of each rat in the experimental treatment groups are presented in the Excel data file 2 available at Mendeley repository.     Fig. 13. Light micrographs of rat kidney structure pretreated with 20 mg/kg AT 30 min prior to the administration of CdCl2. AT protective effect on injury in the kidney tissue, exhibiting normal kidney tissue structure with glomeruli, renal distal convoluted, and collecting duct.

Experimental rats and design
Fifty six adult Wistar male rats weighing between 200 g and 220 g were used in this study. The animals were housed in metal cages, placed 7 rats in each cage under hygienic and standard conditions and temperature maintained at 22 ± 2 °C and 12 h light/dark cycles with free access to rodent food pellets and water. Prior to experiments, rats were acclimatized and all treatments were started after one week.
Cadmium chloride at doses of 1, 2, and 3 mg/kg was dissolved in distilled water and was applied at a volume of 2 ml/kg intraperitoneally. The selected dosages of cadmium chloride were based on prior experiments on toxicity data in animals, where reported the acute intoxication of intraperitoneal injection of various doses of cadmium chloride at 1-3 mg/kg of body weight. These doses indicated biochemical and histopathological dysfunctions following short-term cadmium chloride administration, resulted in adverse effects in kidney [ 1 , 2 ].
Atorvastatin (dose of 20 mg/kg) [ 3 , 4 ] dissolved in the physiologic saline and was administered by an gastric tube (gastric gavages) at a volume of 4 ml/kg. In the previous study statins at a dose of 20 mg/kg revealed potential therapeutic effects against inflammatory diseases in liver and kidney tissues [5] .
Cadmium chloride or its vehicle (normal saline) was used 30 min after the gavage administration of AT or its vehicle. Treatments were within the following timeline: Rats were treated with intra-gastric gavage of saline, AT, or vehicle of AT for 15 days, which started 7 days before intraperitoneal injection of cadmium chloride or its vehicle. On day 16 samples were collected for biochemical and histological analyses.

Rat groupings and treatment
The wistar rats were randomly allocated into eight groups of seven rats in each group. The first group of rats received physiologic saline. The second group treated with oral gavages a dose of 20 mg/ kg /day AT for 15 days. The third, fifth, and seventh groups received cadmium chloride with doses of 1, 2 and 3 mg/kg intraperitoneal (i.p.), while the fourth, sixth, and eighth groups pretreated with oral gavages containing 20 mg AT/kg body weight, 30 minutes prior to the intraperitoneal (i.p.) administration of cadmium chloride at doses of 1, 2 and 3 mg/kg (Excel data file 2 available at mendeley repository). All groups were treated with cadmium chloride for eight consecutive days from day 8 to day 15.
Twenty-four hours after the last treatment, all rats were anesthetized with sodium pentobarbital (50 mg/kg). Blood samples were taken from the heart of animals, and immediately thereafter kidneys were removed, dissected, and washed using normal saline solution. Parts of kidney tissue were removed, fixed and processed for light microscopy, using haematoxylin and eosin (H&E) staining technique. A segment of 0.5 × 0.5 cm 2 of another half was used for the detection of MDA, GSH, SOD, and GPx.

Biochemical analyses
Data collected on cadmium chloride-induced nephrotoxicity by measuring Blood Urea Nitrogen (BUN), and Creatinine (CR) levels in serum. The levels of Malondialdehyde (MDA), Superoxide Dismutase (SOD), Glutathione Peroxidase (GPx) and Glutathione (GSH) in kidney tissue are commonly used to assess oxidative stress. While other enzymatic markers such as N-acetyl-ß-Dglucosaminidase (NAG), ß2G may also be used to estimate renal toxicity, the kits for the above biomarkers were available for the present experiment.
Kidneys tissue was homogenized in phosphate buffered saline, then centrifuged at 800 × g for 10 min at 4 °C and maintained in -80 °C for oxidative stress markers assessment [6] . Blood samples were collected from the heart of animals and the serum was obtained by centrifugation at 30 0 0 rpm for 20 min and stored at −20 °C until the measurement of parameters. Serum concentration of BUN and CR and renal tissues concentration of MDA, GSH, GPx, and SOD were determined according to the related kits instructions. The concentration of Serum BUN was determined colorimetrically using related kits (Pars Azmoon company, Tehran, Iran) according to the method described and Serum Cr was measured by Jaffe's method, using a Commercial Kit (Pars Azmoon Co., Tehran, Iran) [7] . Concentrations of MDA, GSH, GPx, and SOD in kidney tissues were determined as per the instructions of related kits from ZellBio GmbH, Ulm, Germany.
Kidney homogenates were used to evaluate lipid peroxidation by thiobarbituric acid response to MDA Assay Kit (ZellBio GmbH, Ulm, Germany). A combination of homogenate with trichloroacetic acid produces a reactive thiobarbituric acid compound, which is a red complex. The response of the produced red color of the compound was determined at 532 nm using a Nanodrape. This method determines the MDA level with sensitivity equal to 0.1 μM [8] . SOD activity in kidney tissue determined using SOD assay kit (Zellbio Co). In this method, an enzymatic reaction converts superoxide anion to hydrogen peroxide and oxygen. To determine serum GSH and GPx levels, commercial chemical colorimetric assay kits (ZellBio GmbH, Ulm, Germany) were used through colorimetrically method at 412 nm wavelengths. The assay sensitivity was 0.1 mM [9] . GPX activity unit was determined by the amount of the sample that will catalyze 1 μmole GSH to GSSG in one minute. The protein level of in supernatants was assayed by the Bradford method using standard bovine serum albumin at 560 nm [10] .

Histological examinations
Following fixing removed kidney tissues in formalin, a 10 μm section was taken from each tissue block. After making and drying slides, they were stained with haematoxylin and eosin (H&E) method. The criteria for cell injury included nuclear dilation, loss of staining capacity and obvious cellular swelling. In the surface of each slide, five histological fields were randomly selected and photographed under 4 × 100 magnification and evaluated by one pathologist and histologist familiar with experimental procedure.

Statistical data analyses
The data were analyzed using Graphpad Prism 8 computer programs. At first, all of data were analyzed by one-way analysis of variance (ANOVA). Secondly, Tukey's multiple comparisons tests were performed to compare the means of all groups to the mean of every other group. Results were presented as mean ± SE and Probability value of P < 0.05 was determined to be statistically significant.

Ethics statement
All the experimental tests on animals in this study complied with the ARRIVE guidelines (Animal Research: Reporting of In Vivo Experiments) and were carried out in accordance with the National Institutes of Health guide for the care and use of Laboratory animals (NIH Publications No. 8023, revised 1978

Credit Author Statement
AD, EK, ZG, AG, SY contributed to Conceptualization; Data curation; Formal analysis; Investigation; Methodology; Project administration; Resources; Software; Supervision; Validation; Visualization; Writing -original draft; review and editing.

Declaration of Competing Interest
The authors declare that they have no known competing financial interests or personal relationships which have, or could be perceived to have, influenced the work reported in this data article.

Data Availability
Raw and analyzed data of histological alterations and biochemical markers in rat kidney exposed to Cadmium and treated with Atorvastatin (Original data) (Mendeley Data).