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Published on: December 6, 2024
Oxidative stress level in the testes of mice and rats during nickel intoxication
Eugenia Murawska-Ciałowicz1, Wojciech Bal, Lidia Januszewska
1Physiology and Biochemistry Department, University of Physical Education, Avenue I.J. Paderewskiego 35, 51-612 Wroclaw, Poland. eugenia.murawska-cialowicz@awf.wroc.pl
Abstract:
The genotioxic and carcinogenic effect of nickel probably results from its capacity to produce reactive oxygen species (ROS) and disturb the redox balance. The aim of the study was to find out if rats lacking spermatic protamine 2 are less susceptible to Ni(II) than mice. Consequently, the levels of malondialdehyde + 4 hydroxynonenal (MDA+4HDA) - markers of lipid peroxidation, as well as the level of reduced glutathione (GSH) were measured within the rat and mouse testes. Our results showed that the levels of lipid peroxidation markers were elevated in testicular homogenates of intoxicated mice without any changes in rats. GSH level was lower in the group of intoxicated mice comparing to the control without statistically significant changes in rats' homogenates. Moreover, the level of GSH in the testes of intoxicated mice was lower than in rats. On the basis of our results, it appears that Ni(II) can initiate oxidative stress in the testes of mice but not of rats and can reduce GSH level. Consequently, the antioxidative defense of the testes is reduced. Ni(II) that causes oxidative stress in the testes may also contribute to infertility.
Insights
Nickel (Ni(II)) exposure induces oxidative stress and reduces antioxidant defenses in mouse testes, but not in rats. This suggests potential impacts on male fertility due to nickel-induced testicular damage.
Area of Science:
- Toxicology
- Reproductive Biology
- Environmental Health
Background:
- Nickel compounds are known for genotoxic and carcinogenic effects, potentially mediated by reactive oxygen species (ROS) and redox imbalance.
- Oxidative stress is implicated in various pathologies, including male infertility.
Purpose of the Study:
- To investigate the differential susceptibility of rats and mice to nickel(II) (Ni(II)) exposure.
- To assess the impact of Ni(II) on oxidative stress markers and antioxidant levels in rat and mouse testes.
Main Methods:
- Measurement of lipid peroxidation markers (malondialdehyde + 4-hydroxynonenal [MDA+4HDA]) in testicular homogenates.
- Quantification of reduced glutathione (GSH) levels in testicular homogenates.
- Comparison of these markers between control and Ni(II)-exposed rats and mice.
Main Results:
- Lipid peroxidation markers (MDA+4HDA) were significantly elevated in the testes of Ni(II)-exposed mice, but not in rats.
- Reduced glutathione (GSH) levels were significantly decreased in Ni(II)-exposed mice compared to controls.
- GSH levels were lower in Ni(II)-exposed mice testes than in rat testes, indicating reduced antioxidative defense.
Conclusions:
- Ni(II) exposure induces oxidative stress and depletes GSH in mouse testes, compromising antioxidative defense.
- Rats lacking spermatic protamine 2 exhibit resistance to Ni(II)-induced testicular oxidative stress compared to mice.
- Ni(II)-induced oxidative stress in testes may contribute to male infertility.