Lipopolysaccharide Prompts Oxidative Stress and Apoptosis in Rats’ Testicular Tissue

Abstract

Lipopolysaccharide (LPS) is a component of the outer membrane of gram negative bacteria. LPS challenging allows switching transcription of proinflammatory cytokines on via over stimulation of Toll-like receptors (TLRs) signaling pathway with subsequent pathogenic inflammatory response. We investigated the possible reproductive toxicity of LPS in male Wister albino rats. Oxidative stress markers, antioxidant status and caspase-3 activity were analyzed in testicular tissues of rats exposed to either saline or LPS (4 mg/kg BW, ip; 0.18 of the LD 50 ). The samples were collected at 6 h and 72 h after injection of LPS. A significant reduction in testicular reduced glutathione (GSH), glutathione-S-transferase (GST) and superoxide dismutase (SOD) was observed at 72 h compared to control group. Total antioxidant capacity was decreased at 6 h with additional significant reduction at 72 h. Catalase activity was reduced significantly at both 6 and 72 h. Malondialdehyde (MDA) was increased (P ≤ 0.05) in LPS injected rats without variation between 6 and 72 h. A significant increase in nitric oxide (NO) was observed at 72 h after injection. A time-dependent increase in LPS-treated groups was observed in the concentration of caspase-3.Histopathological analysis revealed degenerative changes and necrosis of seminiferous tubules after 6 h with further accumulation of eosinophilic edematous transudate in its lumen after 72 h. In conclusion, by increasing time of exposure, LPS induced lipid peroxidation, oxidative stress, reduced testicular antioxidant capacity and encouraged testicular apoptosis which could be possible mechanisms for impairment of testicular function.

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“…Ayala et al [ 67 ] linked between high levels of free radical and ROS formation and lipid peroxidation. In rats, intraperitoneal injection of LPS driven from E. coli induced lipid peroxidation and reduced glutathione, glutathione-S-transferase and SOD activities as well as TAC with a progressive increasing effect over time [ 68 ]. The cell antioxidant defense includes antioxidant enzymes (e.g., SOD, GPx and catalase) and free radical scavenging antioxidants (e.g., vitamin E and C) in addition to other enzymes and proteins involved in the repair or removal of the damaged molecules (e.g., heat shock proteins, DNA-repairing enzymes and proteasomes) [ 48 ].…”

Salubrious effects of a vermiculite–cellulose‐based bionanocomposite on oxidative stress indices and histomorphology of male Wistar rats

“…ROS signalling has been implicated in cellular maladjustment that could lead to inflammatory responses, with its attendant consequences on spermatogenesis and steroidogenesis (Forrester, Kikuchi, Hernandes, Xu, & Griendling, ; Palladino, Fasano, Patel, Dugan, & London, ). For example, rats exposed to 4 mg/kg bw lipopolysaccharide for 72 hr presented with impaired testicular function, and lipid peroxidation, oxidative stress and depleted antioxidant status were implicated as the possible mechanisms of inflammatory action (Halawa, El‐Adl, Hamed, Balboula, & Elmetwally, ). MPO, located in azurophilic granules of neutrophils, is reportedly discharged during inflammation and testicular damage.…”

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“…Sakkas and El-Fakahany [ 33 ] reported that ROS initiates a cascade of reactions that ultimately trigger apoptosis. Furthermore, some studies have been reported in rats, mice, and humans in which testicular apoptosis was implicated in subfertility and or infertility [ 34 , 35 , 36 , 37 , 38 ]. Venkatesan and Sadiq [ 39 ] reported that the administration of mercury chloride in male rats showed increases in the expression of Bax and caspase-3 and a marked decrease of Bcl-2 level relative to the control group.…”