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Protective effect of hemin against cadmium-induced testicular damage in rats
Amr A Fouad1, Habib A Qureshi, Ali Ibrahim Al-Sultan
1Department of Biomedical Sciences, Division of Pharmacology, College of Medicine, Al-Ahsa, King Faisal University, 31982, Saudi Arabia. amrfouad65@yahoo.com
Insights
Hemin protects against cadmium-induced testicular injury by reducing oxidative stress and inflammation. This heme oxygenase-1 inducer offers a potential therapeutic strategy for testicular protection.
Area of Science:
- Toxicology
- Reproductive Biology
- Biochemistry
Background:
- Cadmium exposure causes testicular injury, characterized by oxidative stress and inflammation.
- Heme oxygenase-1 (HO-1) plays a role in mitigating cellular damage.
Purpose of the Study:
- To investigate the protective effects of hemin, a HO-1 inducer, against cadmium-induced testicular injury in rats.
- To elucidate the underlying mechanisms of hemin's protective action.
Main Methods:
- Testicular damage was induced using a single intraperitoneal injection of cadmium chloride.
- Hemin was administered subcutaneously prior to and during cadmium exposure.
- Biochemical assays measured antioxidant enzyme activities, lipid peroxidation, and inflammatory markers.
- Caspase-3 activity and histological examinations assessed apoptosis and tissue damage.
- The role of HO-1 was confirmed using zinc protoporphyrin-IX, an inhibitor.
Main Results:
- Hemin treatment significantly increased serum testosterone levels, counteracting cadmium-induced reduction.
- Hemin replenished reduced glutathione levels and normalized catalase and superoxide dismutase activities.
- Hemin suppressed cadmium-induced lipid peroxidation and attenuated elevated levels of tumor necrosis factor-alpha and nitric oxide.
- Hemin reduced caspase-3 activity and ameliorated histological damage in testicular tissue.
- The protective effects of hemin were reversed by zinc protoporphyrin-IX, confirming the involvement of HO-1.
Conclusions:
- Hemin exhibits significant protective effects against cadmium-induced testicular toxicity.
- These effects are mediated through hemin's antioxidant, anti-inflammatory, and antiapoptotic properties, primarily via HO-1 induction.
- Hemin represents a promising therapeutic agent for preventing or treating cadmium-related testicular damage.
Abstract:
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.