Protective effect of hemin against cadmium-induced testicular damage in rats.
The protective effect of hemin, the heme oxygenase-1 inducer, was investigated in rats with cadmium induced-testicular injury, in which oxidative stress and inflammation play a major role. Testicular damage was induced by a single i.p. injection of cadmium chloride (2mg/kg). Hemin was given for three consecutive days (40 micromol/kg/day, s.c.), starting 1 day before cadmium administration. Hemin treatment significantly increased serum testosterone level that was reduced by cadmium. Hemin compensated deficits in the antioxidant defense mechanisms (reduced glutathione, and catalase and superoxide dismutase activities), and suppressed lipid peroxidation in testicular tissue resulted from cadmium administration. Also, hemin attenuated the cadmium-induced elevations in testicular tumor necrosis factor-alpha and nitric oxide levels, and caspase-3 activity. Additionally, hemin ameliorated cadmium-induced testicular tissue damage observed by light and electron microscopic examinations. The protective effect afforded by hemin was abolished by prior administration of zinc protoporphyrin-IX, the heme oxygenase-1 inhibitor. It was concluded that hemin, through its antioxidant, anti-inflammatory and antiapoptotic effects, represents a potential therapeutic option to protect the testicular tissue from the detrimental effects of cadmium.
Fouad
Amr A
AA
Department of Biomedical Sciences, Division of Pharmacology, College of Medicine, Al-Ahsa, King Faisal University, 31982, Saudi Arabia. amrfouad65@yahoo.com
Qureshi
Habib A
HA
Al-Sultan
Ali Ibrahim
AI
Yacoubi
Mohamed T
MT
Ali
Abdellah Abusrie
AA
D000818:Animals; D000975:Antioxidants / Q000378:metabolism; D017209:Apoptosis / Q000187:drug effects; D002105:Cadmium Poisoning / Q000473:pathology* / Q000517:prevention & control*; D053148:Caspase 3 / Q000378:metabolism; D020169:Caspases / Q000378:metabolism; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005978:Glutathione / Q000378:metabolism; D051547:Heme Oxygenase-1 / Q000037:antagonists & inhibitors; D006427:Hemin / Q000627:therapeutic use*; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D008854:Microscopy, Electron; D009569:Nitric Oxide / Q000378:metabolism; D016877:Oxidants / Q000378:metabolism; D011524:Protoporphyrins / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D013482:Superoxide Dismutase / Q000378:metabolism; D013733:Testicular Diseases / Q000139:chemically induced* / Q000473:pathology / Q000517:prevention & control*; D013737:Testis / Q000473:pathology / Q000648:ultrastructure; D013739:Testosterone / Q000097:blood; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
D000975:Antioxidants; D004791:Enzyme Inhibitors; D016877:Oxidants; D011524:Protoporphyrins; D014409:Tumor Necrosis Factor-alpha; C017803:zinc protoporphyrin; D009569:Nitric Oxide; D013739:Testosterone; D008315:Malondialdehyde; D006427:Hemin; D051547:Heme Oxygenase-1; D013482:Superoxide Dismutase; D053148:Caspase 3; D020169:Caspases; D005978:Glutathione