RE: Questions/DMSO/ 3 studies

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Pharmacol Res. 2005 Sep;52(3):223-8.

Hepato- and neurotoxicity

induced by thioacetamide: protective effects of

melatonin and dimethylsulfoxide.

Departamento de Bioquimica y Biologia

Molecular, Cordoba, Spain.

The effects of melatonin and dimethylsulfoxide (DMSO)

on liver and brain oxidative stress, hepatic failure and blood urea nitrogen

(BUN) level changes produced by a single dose of thioacetamide

(TAA) in Wistar rats were studies. A dose of either

melatonin (3 mg kg(-1)day(-1)) or DMSO (2 g kg(-1)day(-1))

was injected for 3 days before and for 2 days after the administration of TAA

(150 mg kg(-1) i.p.). Blood samples were taken from

the neck vascular in order to determine ammonium, BUN and liver enzymes. We

estimated lipid peroxidation products, reduced

glutathione (GSH) content and catalase activity in

liver and brain homogenates. TAA caused significant increases in ammonium and

in the levels of aspartate aminotransferase

(AST), alanine aminotransferase

(ALT) and lactate dehydrogenase (LDH) enzymes, while

it decreased BUN values. TAA also increased lipid peroxidation

product levels, but reduced GSH content and catalase

activity in the liver and brain. Both melatonin and DMSO, although melatonin

more significantly, decreased the intensity of the changes produced by the

administration of TAA alone. Furthermore, melatonin alone or combined with TAA

increased the BUN levels and decreased the ammonia values compared with control

animals. These results support the antioxidative and neuro-/hepato-protective action of melatonin and a lesser

action of DMSO. Likewise, these data seem to support the hypothesis of an

effect of melatonin on urea synthesis.

PMID: 15896975 [PubMed - indexed for MEDLINE]

Acta Chir Belg.

2003 Aug;103(4):392-5.

The effects of dimethylsulfoxide in

experimental obstructive jaundice.

Department of

Surgery, Erciyes University School of Medicine, Kayseri, Turkey.

MATERIAL AND METHODS: Thirty rats were divided into

three groups, as sham, control and DMSO groups. Laparatomy

was performed on each animal in the control and DMSO groups and common bile

ducts were ligated. Common bile duct was observed but

was not ligated for the rats in the sham group.

Saline solution injection (1.5 mg/kg/intraperitoneally

(i.p.)) was begun on the first day of surgical

procedure and repeated once a day for the next 5 days. The same procedure was

performed with DMSO (1.5 mg/kg/i.p.) instead of

saline in the DMSO group. The rats were sacrificed on the postoperative seventh

day, at which time venous blood and liver tissue specimens were taken. MAIN

OUTCOME MEASUREMENTS: On the 7th postoperative day, the bilirubin,

AST, ALT, ALP and GGT levels of the control and DMSO groups were significantly

higher in comparison with the sham group (p < 0.01). On the 7th

postoperative day, the erythrocyte superoxide dismutase (SOD) and glutathione peroxidase

(GSH-Px) levels of the control and DMSO groups were

significantly lower than those of the sham group (p < 0.01), but there was

no statistical difference between the two groups (p > 0.05). Erythrocyte and

liver malondialdehyde (MDA) levels in the control and

DMSO groups were significantly higher compared with the sham group (p <

0.01). However, the MDA levels were significantly lower in the DMSO group

compared to the control group (p < 0.01). CONCLUSION: It is stated that free

oxygen radicals seem to play a role in the liver tissue injury, secondary to

obstructive jaundice. In our experimental study, exogenic

DMSO seems to have decreased lipid peroxidation and

to have improved some of the parameters of liver tissue injury due to the

obstructive jaundice in rats.

PMID: 14524158 [PubMed - indexed for MEDLINE]

Transplant

Proc. 2004 Nov;36(9):2590-2.

The effects of dimethyl sulfoxide on liver damage caused by ischemia-reperfusion.

Department of

General Surgery, Selcuk University,

Medical Faculty, Konya, Turkey.

INTRODUCTION: The aim of this study was to investigate the effects of dimethyl sulfoxide on liver

damage caused by ischemia-reperfusion after portal vein clamping. MATERIAL AND

METHODS: Forty New Zealand

rabbits were divided into three groups with the portal veins of all the rabbits

except the sham group clamped for 30 minutes: group I, sham procedure; group

II, control group; and group III, 500 mg/kg DMSO. The drug was administered IM

in the left inguinal region 30 minutes before the operation. Blood samples (5 mL) were taken from the animals at 15, 30, and 45 minutes.

At the end of the experiment 1 g of liver tissue samples were obtained. Malondialdhyde (MDA), nitric oxide (NO), AST, ALT, and LDH

plasma levels were measured in the blood samples. Liver tissue samples stained

with hematoxylin eosin were examined under light

microscopy for histopathological changes. FINDING:

The liver enzymes in both clamping groups increased significantly compared with

the sham group (P < .01). Enzyme levels of the DMSO group decreased

significantly compared to the control clamping group (P < .05). Similar to

the enzyme changes, MDA and NO levels increased in the portal vein clamping versus

the sham group and decreased in the drug-administered group versus the control

clamped group (P < .03). The severity of histopathological

changes was less in the DMSO group than in the clamped controls. CONCLUSION:

DMSO decreased the severity of liver damage after portal vein clamping.

PMID: 15621097 [PubMed - indexed for MEDLINE]

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