Vitamin E against oxidative damage caused by formaldehyde in frontal cortex and hippocampus: biochemical and histological studies.
Formaldehyde (FA) can cause severe central nervous system impairment. But, there are only a few studies about biochemical and histopathological changes of frontal cortex and hippocampal tissue caused by FA toxicity. The aim of our study was to investigate these changes occurring after chronic formaldehyde toxicity in frontal cortex and hippocampal tissues, and protective effect of Vitamin E (vit E) against oxidative damage. Eighteen rats were divided into three groups: (1) control, (2) treated with FA (FAt), and (3) treated with FA and vit E (FAt+vit E) groups. After the treatment, the animals were sacrificed and frontal cortex and hippocampal tissues were removed for biochemical and histopathological investigation. FA significantly increased tissue malondialdehyde (MDA) and protein carbonyl (PC) levels and also decreased superoxide dismutase (SOD) and catalase (CAT) enzyme activities in frontal cortex and hippocampal tissue compared to control. Vit E treatment decreased MDA and PC levels and prevented inhibition of SOD and CAT enzymes in the tissues. In the FAt group, the neurons of both tissues became extensively dark and degenerated with picnotic nuclei. The morphology of neurons in FAt+vit E group was protected well, but not as neurons of the control group. The number of neurons in frontal cortex and hippocampal tissue of FAt group was significantly less than both control and FAt+vit E groups. It was concluded that vit E treatment might be beneficial in preventing FA-induced oxidative frontal cortex and hippocampal tissue damage, therefore, shows potential for clinical use.
Gurel
Ahmet
A
Department of Biochemistry, Zonguldak Karaelmas University, Faculty of Medicine, 67600 Kozlu, TR-44069 Zonguldak, Turkey. dragurel@yahoo.com
Coskun
Omer
O
Armutcu
Ferah
F
Kanter
Mehmet
M
Ozen
Oguz Aslan
OA
D000818:Animals; D000975:Antioxidants / Q000494:pharmacology* / Q000627:therapeutic use; D001921:Brain / Q000187:drug effects* / Q000473:pathology / Q000503:physiopathology; D002374:Catalase / Q000378:metabolism; D005557:Formaldehyde / Q000037:antagonists & inhibitors* / Q000633:toxicity; D005625:Frontal Lobe / Q000187:drug effects / Q000473:pathology / Q000503:physiopathology; D006624:Hippocampus / Q000187:drug effects / Q000473:pathology / Q000503:physiopathology; D008315:Malondialdehyde / Q000378:metabolism; D009336:Necrosis / Q000139:chemically induced / Q000473:pathology / Q000517:prevention & control; D009410:Nerve Degeneration / Q000139:chemically induced / Q000473:pathology / Q000517:prevention & control*; D018696:Neuroprotective Agents / Q000494:pharmacology / Q000627:therapeutic use; D009498:Neurotoxins / Q000037:antagonists & inhibitors / Q000633:toxicity; D018384:Oxidative Stress / Q000187:drug effects* / Q000502:physiology; D051381:Rats; D017208:Rats, Wistar; D013482:Superoxide Dismutase / Q000378:metabolism; D016896:Treatment Outcome; D014810:Vitamin E / Q000494:pharmacology* / Q000627:therapeutic use
D000975:Antioxidants; D018696:Neuroprotective Agents; D009498:Neurotoxins; D014810:Vitamin E; D005557:Formaldehyde; D008315:Malondialdehyde; D002374:Catalase; D013482:Superoxide Dismutase