Cell and Tissue Journal

Abstract Introduction: Oxidative stress exerts destructive effects on sperm cells, leading to sperm dysfunction and male infertility. It occurs when there is an imbalance between the production of reactive oxygen species (ROS) and the cell's antioxidant defense system. ROS are free radicals and peroxides that can damage cells. They can harm the sperm cell membrane, which is rich in polyunsaturated fatty acids, through lipid peroxidation, impairing sperm membrane fluidity. This affects motility and the sperm's ability to fuse with the egg. Additionally, ROS can directly damage sperm DNA, leading to DNA fragmentation and other abnormalities. Oxidative stress can also impair sperm motility by disrupting energy production in the mitochondria. Severe oxidative stress may result in sperm cell death (apoptosis or necrosis), reducing sperm viability. These negative effects ultimately decrease the chances of successful fertilization and a healthy pregnancy.
Cadmium, a pervasive environmental and industrial pollutant, induces significant toxic effects on human health, particularly on the male reproductive system. It is both a naturally occurring element and a widespread environmental pollutant generated from various industrial and agricultural activities. Its presence in soil, water, air, and food exert risks on human health. Exposure to cadmium is strongly linked to increased oxidative stress, which damages cellular components such as lipids, proteins, and DNA within sperm cells. This oxidative damage can lead to impairments in critical sperm parameters, including motility, viability, morphology, and DNA integrity, thereby compromising fertilization potential and contributing to male infertility. The severity of these effects underscores the need for effective strategies to mitigate cadmium-induced sperm damage.
Alpha-lipoic acid (ALA), a naturally occurring organosulfur compound, is produced in the body, obtained through dietary sources, and taken as a supplement or medication. ALA is a potent antioxidant with the unique ability to function in both aqueous and lipid environments. This versatility allows ALA to scavenge a wide range of free radicals and ROS, thereby protecting cells from oxidative damage. Furthermore, ALA can regenerate other endogenous antioxidants, such as glutathione, further amplifying its protective effects. Given ALA’s well-documented antioxidant properties and its potential to mitigate oxidative stress, this study aims to investigate its protective effects on human sperm exposed to cadmium.
Aim: This research will explore the extent to which ALA can counteract the detrimental effects of cadmium-induced oxidative stress on vital sperm parameters. By evaluating the impact of ALA supplementation on sperm motility, viability, morphology, and DNA integrity in the presence of cadmium, this study seeks to determine the potential therapeutic role of ALA in preserving sperm function and improving male fertility outcomes. The results of this investigation will provide valuable insights into the efficacy of ALA as a protective agent against cadmium-induced reproductive toxicity and contribute to the development of strategies for mitigating the harmful effects of environmental pollutants on male reproductive health.
Materials and Methods: In this experimental study, human sperm samples were divided into five groups: 1) spermatozoa at 0 hours, 2) spermatozoa at 180 minutes (control group), 3) spermatozoa treated with cadmium chloride (10 μM) for 180 minutes, 4) spermatozoa treated with ALA (50 μM) + cadmium chloride (10 μM) for 180 minutes and 5) spermatozoa treated with ALA (50 μM) for 180 minutes.
Vital sperm parameters, including motility, viability, plasma membrane and acrosome integrity, mitochondrial membrane potential, and DNA fragmentation, as well as oxidative stress indices (total antioxidant capacity and lipid peroxidation), were examined in different groups. Data were expressed as mean ± standard deviation and analyzed using one-way analysis of variance (ANOVA). Means with p

Abstract Aim: Organotypic cultures of spinal cord slices from mammalian neonatal and fetal animals are powerful tools for studies of spinal cord injury, neuronal degeneration, and cell death but also motor neuron regeneration. Models in which adult slices are used would be very useful. However, adult spinal cord slices are notoriously difficult to maintain in culture and rapidly deteriorate in vitro. Degeneration of motor neurons in the spinal cord is a critical phenomenon in spinal cord injuries and certain neurodegenerative diseases such as amyotrophic lateral sclerosis, a neurodegenerative disorder in which motor neurons in the spinal cord and motor cortex are lost. A variety of mechanisms have been proposed as having a role in neuronal apoptosis during spinal cord injury. Oxidative stress has been reported as one of the mechanisms involved in the apoptosis of motor neurons in spinal cord injuries and neurodegenerative diseases. This study was conducted to determine whether quercetin, as a potent antioxidant, can delay apoptosis in motor neurons of cultured spinal cords by reducing oxidative stress.
 Material and methods: The thoracic regions of the spinal cord from adult NMRI mice were sliced using a tissue chopper and divided into three groups: 1) 0-hour, 2) control group, and 3) group treated with quercetin (100 µM). Spinal cord slices in the 2 and 3 groups were incubated for 6 hours at 37°C in a Co₂ incubator. The viability of the spinal cord slices was measured using MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) assay. The morphological features of apoptosis and the number of motor neurons were examined using Hoechst and propidium iodide staining. The malondialdehyde was measured to determine lipid peroxidation while the FRAP (ferric reducing antioxidant power) was assessed to evaluate total antioxidant capacity in fresh and cultured spinal cord slices. Results were expressed as mean±SD. One-way analysis of variance (ANOVA) followed by Tucky’s test was used to assess the statistical significances of the data. In all cases, a statistical probability of p<0.05 was considered significant.
Results: After 6 hours (control group) in culture, the viability of the spinal cord slices, the neuron diameter, and the number of healthy motor neurons significantly decreased compared to the 0-hour group. Also, motor neurons showed the morphological features of apoptosis including cell shrinkage, nuclear and chromatin condensation in the control group. A significant increase in the amount of malondialdehyde and a significant decrease in the total antioxidant capacity was also observed compared with the 0-hour group. After 6 hours, quercetin not only increased the viability and the number of healthy motor neurons in the cultured slices but also reduced the morphological features of apoptosis in the motor neurons compared with the control group. In addition, quercetin significantly reduced the amount of malondialdehyde and increased the total antioxidant power in slices cultured for 6 hours.
Conclusion: Oxidative stress might be considered as one of the mechanisms involved in the apoptosis of motor neurons in cultured spinal cord slices and quercetin, as a potent antioxidant, was able to increase the viability of the cultured spinal cord slices and delay the morphological features of apoptosis in the motor neurons through reducing lipid peroxidation and increasing the total antioxidant capacity.