Monosodium glutamate exacerbated the lipopolysaccharide-induced reproductive toxicity of male Wistar rats.

Abstract

Background: Monosodium glutamate (MSG) is a common food additive that has been linked to oxidative stress and reproductive dysfunction. Lipopolysaccharide (LPS), a bacterial endotoxin, is known to induce systemic inflammation, leading to oxidative damage and hormonal disruption. This study investigated whether MSG exacerbates LPS-induced testicular toxicity in male Wistar rats via oxidative stress and endocrine dysfunction.

Methods: Twenty-eight male Wistar rats were divided into four groups (n = 7): control (distilled water), MSG (1500 mg/kg), LPS (250 µL/kg), and a combination of MSG + LPS. MSG was used in the background of LPS to model a real-life "double-hit" exposure where dietary and microbial toxins co-exist. We hypothesised that MSG would amplify LPS-induced reproductive damage through converging mechanisms such as ROS generation, antioxidant depletion, and hormonal dysregulation.

Results: Compared to control, MSG and LPS significantly reduced sperm count (MSG: p = 0.0001; LPS: p = 0.0001), motility (p = 0.0001; p = 0.0001), and viability (p = 0.0001; p = 0.0001), with more pronounced effects in the MSG + LPS group (p = 0.0001). The number of abnormal sperm cells was, however, increased significantly (p = 0.0001 for MSG; p = 0.0001 for LPS; p = 0.0009 for MSG + LPS). Serum testosterone (p = 0.0001 for MSG; p = 0.0001 for LPS; p = 0.0001 for MSG + LPS), FSH (p = 0.0001, 0.0001, 0.0001), and LH (p = 0.0001, 0.0001, 0.0001) were significantly decreased. Antioxidant enzymes/parameter SOD (p = 0.0001, 0.0001, 0.0001), CAT (p = 0.0001, 0.0001, 0.0001), GST (p = 0.0001, 0.0001, 0.0001), and GSH (p = 0.0001, 0.0001, 0.0001) were depleted, while TBARS levels increased significantly (p = 0.0001, 0.0001, 0.0001). Histological analysis revealed extensive structural damage in the MSG + LPS group.

Conclusions: These findings suggest that MSG potentiated LPS-induced testicular toxicity through oxidative stress and endocrine suppression, underscoring potential reproductive risks associated with combined dietary and inflammatory exposures.