***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: BACKGROUND : Cisplatin ( CP ) as a potential drug for solid tumors produces nephrotoxicity and disturbs endothelial function . CP induced nephrotoxicity may be gender related . Nitric oxide plays a pivotal role in endothelial function and L-arginine as endogenous NO donor promotes endothelial function . The role of L-arginine in CP induced nephrotoxicity model and its gender related was investigated in this study . METHODS : Thirty three Wistar rats were r and omly assigned to four groups . The groups 1 ( male , n = 6 ) and 2 ( female , n = 11 ) received a single dose of L-arginine ( 300 mg/kg , ip ) , and the day after , they received a single dose of CP ( 7 mg/kg ) . The group 3 ( male , n = 9 ) and 4 ( female , n = 7 ) were assigned to the same regimen except for saline instead of L-arginine . All animals were sacrificed one week after CP administration . The levels of blood urea nitrogen ( BUN ) , creatinine and nitrite were measured . The kidneys were also removed for pathological investigations . RESULTS : Five animals died . All CP treated animals lost weight . The normalized weigh loss was significantly different between male and female in CP+L-arginine treated animals ( p < 0.05 ) . BUN and creatinine were increased significantly in male treated with CP and in female treated with CP+L-arginine ( p < 0.05 ) . L-arginine  reduced BUN in male ( not in female ) when compared with control groups ( p < 0.05 ) . The level of nitrite was increased significantly in L-arginine treated animals . Kidney tissue damage score and normalized kidney weight were greater in females treated with CP+ L-arginine than female received CP alone ( p < 0.05 ) . CONCLUSIONS : L-arginine may protect against CP induced nephrotoxicity in male , but it promotes the induced damage in female . The exact mechanism need to be defined Objectives : Cisplatin ( CP ) is used as the commonest drug to treat solid tumors . It is accompanied by a nephrotoxicity side effect . The main objective of this study is to investigate the protective role of magnesium ( Mg ) supplementation in CP-induced nephrotoxicity in a rat model . Methods : Twenty-nine Wistar rats were r and omly assigned to four groups ( 1–4 ) . Groups 1–3 received 20 , 80 , and 200 mg/kg magnesium sulfate respectively , for 10 days , but on day 3 , a single dose of CP ( 7 mg/kg , i.p . ) was also injected . Group 4 ( positive control group ) received the same regimen of Groups 1–3 except saline instead magnesium sulfate . One week after CP administration , blood sample s were obtained and all animals were killed for kidney histopathological investigations . Results : All CP-treated animals lost weight , and the percentage of weight loss in Group 1 ( low dose Mg sulfate treated ) was significantly higher compared with the positive control group ( Group 4 , P < 0.05 ) . The increase in blood urea nitrogen ( BUN ) and creatinine ( Cr ) levels in serum in Group 1 were more than those in other groups ( P < 0.05 ) . No statistical differences were observed in serum magnesium , nitrite , and total protein levels among the groups . The kidney tissue damage in Groups 1–3 was not significantly different when compared with Group 4 . Moreover , the kidney and testis weights in Group 1 were significantly greater than those in the positive control group ( P < 0.05 ) . Conclusion : Regarding the BUN and Cr levels in the serum , kidneys weight , and the histopathological study , the low dose of Mg supplementation intensifies kidney toxicity and renal dysfunction in CP-induced nephrotoxicity in the rat model . However , the protective role of Mg with moderate and high doses is not certain PURPOSE Serious cumulative toxicity is a well-recognized consequence of chemotherapy . Amifostine , an organic thiophosphate , has demonstrated the ability to protect selectively a broad range of normal , but not neoplastic , tissues from the cytotoxic effects of chemotherapy and radiotherapy . This study was design ed to determine if amifostine could reduce the serious toxicities associated with cyclophosphamide and cisplatin ( CP ) , without reducing antitumor efficacy in patients with ovarian cancer . PATIENTS AND METHODS Two hundred forty-two patients with advanced ovarian cancer were r and omized to receive six cycles of cyclophosphamide ( 1,000 mg/m2 ) and cisplatin ( 100 mg/m2 ) with or without amifostine ( 910 mg/m2 ) every 3 weeks for six cycles . The occurrence of hematologic , renal , neurologic , and ototoxicity was evaluated . Antitumor efficacy was assessed by pathologic tumor response and survival . RESULTS Pretreatment with amifostine before each cycle of chemotherapy result ed in a reduction of cumulative toxicities . Hematologic toxicity consisted of grade 4 neutropenia associated with fever and /or infection that required antibiotic therapy ( P = .005 ) , days in hospital ( P = .019 ) , and days on antibiotics ( P = .031 ) . Platinum-specific toxicities consisted of protracted serum creatinine elevations ( P = 0.004 ) , > or = 40 % reduction from baseline in creatinine clearance ( P = .001 ) , and severity of neurologic toxicity ( P = .029 ) . Twenty-four percent of  CP  patients compared with 9 % of amifostine plus CP patients discontinued therapy because of protocol -specified toxicity ( P = .002 ) . Pathologic tumor response rates were 37 % with amifostine and 28 % in controls , with comparable median survival times of 31 months . Amifostine was generally well tolerated ; the principal side effects were emesis and a transient decrease in blood pressure . CONCLUSION Pretreatment with amifostine reduces the cumulative hematologic , renal , and neurologic toxicities associated with the CP regimen , with no reduction in antitumor efficacy The aim of this study was to compare the roles of dihydropyridine calcium antagonists nifedipine , nitrendipine , amlodipine on doxorubicin (DXR)-induced nephrotoxicity in rats using biochemical , histopathological and immunohistochemical approaches . Male Sprague-Dawley rats were r and omly divided into five experimental groups : control ; DXR ; DXR+nifedipine ( 15 mg/kg ) ; DXR+nitrendipine ( 10 mg/kg ) ; DXR+amlodipine ( 5 mg/kg ) . Results showed that treatment with DXR alone caused significant changes in the levels of urinary protein , serum creatinine ( SCr ) , and blood urea nitrogen ( BUN ) . Co-administration with amlodipine effectively reversed the effect of DXR on these parameters . In contrast , nifedipine and nitrendipine either had no effect or worsened DXR induced changes in the levels of urinary protein , SCr and BUN . Furthermore , DXR treatment caused significant increases in the levels of malondialdehyde ( MDA ) , nitric oxide ( NO ) , nitric oxide synthase ( NOS ) and significant decreases in the levels of reduced glutathione ( GSH ) , glutathione-S-transferase ( GST ) , and superoxide dismutase ( SOD ) . These effects were significantly reduced by co-administration with amlodipine but not affected by nifedipine and worsened by nitrendipine . In addition to the biochemical changes , histopathological studies showed that DXR caused significant structural damages in the kidneys . Glomerular cell apoptosis , a decrease in Bcl-2 expression and an increase in Bax expression were observed in all rats treated with DXR . Co-administration with amlodipine effectively reversed the effect of DXR while nifedipine and nitrendipine had no effect . In conclusion , this study clearly indicated that amlodipine protected against DXR-induced nephrotoxicity while nifedipine and nitrendipine had no effect Cisplatin is a potent and a major anti-neoplastic drug in the treatment of a broad spectrum of malignancies . However , its clinical use is limited by renal tubular dysfunction that occurs in a significant percent of patients . The aim of the present study was to evaluate the possible protective effect of theophyline in the prevention of cisplatin-induced nephrotoxicity . The trial design was prospect i ve , r and omized , double-blinded and placebo controlled . Chemotherapeutic patients who received cisplatin at a dosage of at least 50 mg/m 2 alone or in combination with other chemotherapy agent(s ) were included in the study . There were a total of 76 patients who were r and omly divided into two groups . In group 1 ( n = 38 ) , placebo was advised ; in group 2 ( n = 38 ) , patients received 4 mg/kg aminophyline as an intravenous loading dose , followed by theophyline in a dose of 200 mg three times daily orally for four consecutive days . The  placebo group had 22 males and 16 females and the theophyline group had 26 males and 12 females . The mean age was 51 ± 17.6 years and the mean dose of cisplatin was 86.71 ± 43.18 mg .  The prevalence of cisplatin nephrotoxicity in groups 1 and 2 was 7.9 and 5.3 % , respectively , and the difference was not significant ( P = 1 ) . In addition , there was no significant association of cisplatin nephrotoxicity with age ( P = 0.1 ) , gender ( P = 0.64 ) and mean dose of cisplatin ( P = 0.8 ) . These results indicate that prophy-lactic application of aminophyline and theophyline does not have a protective effect against cisplatin nephrotoxicity Nephrotoxicity is the main secondary effect of cyclosporine A ( CsA ) treatment . The antioxidant action of Nigella sativa oil ( NSO ) may explain the protective effect of these agents against various hepatotoxic and nephrotoxic models in vivo and in vitro . This study was design ed to investigate the possible protective effects of NSO , in prevention of chronic CsA-induced nephrotoxicity in rats . Animals were r and omly divided into four experimental groups : the control group received sunflower oil , the other groups were treated with CsA ( 25 mg/kg/day b.w . orally ) or NSO ( 2 ml/kg orally ) or CsA + NSO , respectively . Urine and serum creatinine levels , tissue superoxide dismutase , glutathione peroxidase and catalase enzyme activities , and nitric oxide and malondialdehyde levels were measured , and histological examination was performed . In our study , CsA caused a significant deterioration in the renal function , morphology and gave rise to severe oxidative stress in the kidney . NSO significantly improved the functional and histological parameters and attenuated the oxidative stress induced by CsA. In conclusion , our study demonstrated for the first time that NSO protects kidney tissue against oxygen free radicals , preventing renal dysfunction and morphological abnormalities associated with chronic CsA administration This study aims to evaluate efficacy and safety of Nigella sativa oil supplementation in patients with chronic kidney disease Stage 3 and 4 due to diabetic nephropathy . It was a prospect i ve , comparative , and open-label study . Patients were r and omized into two groups . Group 1 ( Control ) received conservative management of diabetic nephropathy , whereas Group 2 ( Test ) received N. sativa oil ( 2.5 mL , once daily and per orally ) along with conservative management for 12 weeks .  Blood glucose , hemogram , and kidney function test were done at 0 , 6 , and 12 weeks of treatment . Significance of differences between pre- and post-treatment values in each group was assessed using Student 's paired t-test and between the groups using unpaired t-test . We found a drop in blood glucose , serum creatinine , blood urea , and 24 h total urinary protein levels and a rise in glomerular filtration rate , 24 h total urinary volume , and hemoglobin level in the treatment group compared to the control group BACKGROUND Experimental evidence s have demonstrated that Nigella sativa Linn . seed ( NS ) has positive modulation effects on aged rats with memory impairments , prevents against hippocampal pyramidal cell loss and enhances consolidation of recall capability of stored information and spatial memory in rats .  NS has neuroprotective , nephroprotective , lung protective , cardioprotective , hepatoprotective activities as established by previous studies on animals . Several clinical trials with NS on human have also demonstrated beneficial effect . AIM OF THE STUDY The present study was design ed to investigate the effects of NS on memory , attention and cognition in healthy elderly volunteers . Furthermore , safety profile of NS was assessed during the nine-week study period . METHODS Forty elderly volunteers were recruited and divided r and omly into group A and group B -- each consisting of 20 volunteers . The treatment procedure for group A was 500 mg NS capsule twice daily for nine weeks and Group B received placebo instead of NS in the similar manner . All the volunteers were assessed for neuropsychological state and 
    Output:
    
Experimental animal studies showed the protective effect of NS , or TQ  , on  chemotherapy-induced nephrotoxicity .
These effects are caused by decreasing lipid peroxidation and increasing activity of antioxidant enzymes in renal tissue of chemotherapy-treated animals