There is increasing evidence that oxidative stress, due to estrogen deficiency, leads to osteopenia. In this study, dimethyl sulfoxide (DMSO), an antioxidant solvent, was used against post-ovariectomy osteopenia (PO) in rats. Forty female rats were divided into 5 groups randomly as follows: Sham, control group; OVX, ovariectomized group; DMSO1, ovariectomized injected DMSO (0.5 ml/kg/d ip); DMSO2, ovariectomized injected DMSO (1 ml/kg/day ip) and DMSO3, ovariectomized injected DMSO (2 ml/kg/d ip). DMSO therapy started 1 week after ovariectomy and continued for 13 weeks. After 13th weeks, sera were prepared, and then L4 vertebrae and right tibial bones rinsed in fixative. Serum bone alkaline phosphatase (BALP), osteocalcin, pyridinoline, malondialdehyde (MDA) and glutathione (GSH) were measured. Trabecular volume density, trabecular and cortex thickness were estimated. Osteoclast and osteoblast numbers were counted morphometrically. The data were analyzed by ANOVA and then post hoc Tukey test at p < 0.05. The increase of pyridinoline and decrease of BALP in DMSO injected groups were inhibited compared with OVX group (p < 0.05). In DMSO injected groups, decrease of bone density, trabecular volume density, thickness of trabecular and tibial cortex were inhibited compared with OVX group (p < 0.05). MDA decreased significantly in DMSO injected groups compared with OVX group. Osteoclast number decreased in DMSO injected groups compared with OVX group (p < 0.05). Osteoblast number did not show significant change in DMSO groups compared with OVX group. In conclusion, DMSO ameliorates PO through decrease of osteoclast number, osteoclast inhibition and osteoblast activation. These effects may probably be mediated via antioxidant property of DMSO.
Introduction: Gentamicin sulphate (GS) induces nephrotoxicity by increasing of reactive oxygen species (ROS). Objectives: The aim of this research was to assess the renoprotective effect of dimethyl sulfoxide (DMSO) as an antioxidant agent against GS-induced nephrotoxicity. Materials and Methods: Forty male rats (Sprague-Dawley) were divided equally in to five groups and were treated as follows; group 1; received normal saline and served as normal controls, group 2; received GS (100 mg/kg/d), groups 3; received GS and DMSO (0.5 mL/kg/d), groups 4; received GS and DMSO (1 mL/kg/d), groups 5; received GS and DMSO (2 mL/kg/d). After eight days of treatment, serum was prepared. Paraffin sections (3 µ thickness) were prepared from the left kidneys and stained through periodic acid-Schiff (PAS) method. Serum creatinine and urea were assessed by the kits and serum malondialdehyde (MDA) was assessed by thiobarbituric acid (TBA) test. Volume density of proximal tubules, tubular necrosis, tubular cast and lymphocyte infiltration were evaluated histopathologically. The data were analyzed by Mann-Whitney U test at P< 0.05 by SPSS 12 software. Results: Serum MDA, creatinine, urea, tubular volume density, tubular necrosis, tubular cast and lymphocyte infiltration were ameliorated significantly in groups four and five compared with group two (P<0.05). Conclusion: DMSO improved GS-induced renal toxicity significantly through prevention of lipid peroxidation and inflammation, but could not save kidney functional tests and histological changes at the same level as that of the normal group.
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