Background/AimsThis study aimed to investigate the effect of lutein on methotrexate (MTX)-induced pulmonary toxicity in rats biochemically and histopathologically.MethodsThe rats in the MTX + lutein (MTXL, n = 6) group were given 1 mg/kg of lutein orally. A 0.9% NaCl solution was administered orally to the MTX (n = 6) group and the healthy group (HG, n = 6). One hour later, a single 20 mg/kg dose of MTX was injected intraperitoneally in the MTXL and MTX. Lutein or 0.9% NaCl solution was administered once a day for 5 days. At the end of this period, malondialdehyde (MDA), myeloperoxidase (MPO), total glutathione (tGSH), interleukin 1 beta (IL-1β), and tumor necrosis factor alpha (TNF-α) were measured in the lung tissues from the animals euthanized with 50 mg/kg thiopental sodium anesthesia. Subsequently, histopathological examinations were performed.ResultsThe levels of MDA, MPO, IL-1β, and TNF-α in the lung tissue of the MTX were significantly higher than those of the MTXL and HG groups (p < 0.0001), and the amount of tGSH was lower. The histopathological findings in the MTX group, in which the oxidants and cytokines were higher, were more severe.ConclusionsLutein prevented the MTX-induced oxidative lung damage biochemically and histopathologically. This result indicates that lutein may be useful in the treatment of MTX-induced lung damage.
The effects of extracorporeal shock wave lithotripsy (ESWL) on patients undergoing ESWL for renal stone treatment have been studied using activities of glucose-6-phosphate dehydrogenase (G6PDH), superoxide dismutase (SOD) and catalase (CAT), and levels of malondialdehyde (MDA) in the erythrocyte haemolysate. The study included 23 patients (eight women, 15 men with an age range of 23-57 years). Blood samples were taken 5 min before ESWL, in addition to 1 h and 5 days after termination of treatment. Enzyme activities and MDA levels in erythrocytes were measured spectrophotometrically. When compared with the values obtained before ESWL, erythrocyte G6PDH (p = 0.015), SOD (p = 0.036) and CAT (p = 0.01) activities were found to be significantly reduced at the first hour after ESWL. On the fifth day after ESWL, erythrocyte enzyme activities were normalized to the values obtained before ESWL. Although there was a significant difference between values before and 1 h after ESWL (p = 0.003), no difference was detected between 1 h after ESWL and 5 days after ESWL (p > 0.05) in terms of MDA values. The findings of the present study revealed that erythrocyte lipid peroxidation might be induced and antioxidative defence mechanism may be transiently impaired by ESWL.
Thiamine pyrophosphate (TPP) is the active metabolite of thiamine. This study aimed to
investigate the effects of thiamine and TPP on cisplatin-induced peripheral neuropathic
pain (PNP). Male albino Wistar type Rattus norvegicus were divided into
six groups (n=6) that received 2 mg/kg cisplatin (CIS), 25 mg/kg thiamine (TM), 2 mg/kg
cisplatin+25 mg/kg thiamine (CTM), 25 mg/kg TPP (TPP), 2 mg/kg cisplatin+25 mg/kg TPP
(CTPP), or distilled water (healthy group; HG) for 8 days intraperitoneally. Analgesic
effect was measured with a Basile Algesimeter. IL-1β, malondialdehyde
(MDA), total glutathione (tGSH), thiamine, and TPP were determined in blood samples.
Histopathological examinations were performed on removed sciatic nerves. The percent
analgesic effects of the CTM and CTPP groups were calculated to be 21.3% and 82.9%,
respectively. Increased production of IL-1β and MDA by cisplatin was
inhibited by TPP, while it was not inhibited by thiamine. Conversion of thiamine to TPP
significantly decreased in the CIS group. Histopathological and biochemical investigations
demonstrated that hyperalgesia and sciatic nerve damage developed in the CIS and CTM
groups with low TPP levels. These results indicate that cisplatin inhibits the formation
of TPP from thiamine, leading to severe PNP. This finding suggests that TPP may be more
beneficial than thiamine for the treatment of cisplatin-induced PNP.
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