Furkan Aykurt

Cadmium (Cd) is a highly toxic heavy metal that accumulates primarily in the kidneys, where it induces oxidative stress, inflammation, and cellular damage. Cd exposure is a major environmental and occupational concern due to its persistence and bioaccumulative nature. Morin, a natural flavonoid abundant in various fruits and medicinal plants, possesses potent antioxidant and anti-inflammatory properties. However, its potential protective efficacy against Cd-induced nephrotoxicity has not been fully elucidated. This study aimed to evaluate the protective effects of Morin against Cd-induced oxidative and inflammatory damage in rat kidney tissue and to assess its association with oxidative stress and inflammatory responses. Fifty adult male Sprague-Dawley rats were randomly divided into five groups: Control, Cd (6.5 mg/kg, i.p.), Morin100+Cd (100 mg/kg Morin + Cd), Morin200+Cd (200 mg/kg Morin + Cd), and Morin200 (200 mg/kg Morin alone). Cadmium was administered intraperitoneally for 5 consecutive days, while Morin was given intragastrically one hour before Cd injection. Cadmium exposure significantly elevated malondialdehyde (MDA) levels and proinflammatory cytokines (TNF-α, IL-1β, IL-6, IFN-γ) while reducing the activities of antioxidant enzymes (SOD, CAT, GPx, GSH) and anti-inflammatory cytokines (IL-10, IL-4). Morin treatment, particularly at 200 mg/kg, markedly ameliorated these alterations by suppressing oxidative stress, restoring antioxidant enzyme activities, and modulating cytokine balance. These findings indicate that Morin exerts a strong nephroprotective effect against Cd-induced renal toxicity through attenuation of oxidative stress and inflammation, possibly associated with its antioxidant and anti-inflammatory properties. Therefore, Morin may represent a promising natural therapeutic candidate for the prevention of heavy metal-induced renal injury.

Glyphosate (GLY) is a widely used herbicide known to exert toxic effects on the male reproductive system. Boric acid (BA), possessing antioxidant and anti-inflammatory properties, has been investigated for its potential protective effects against oxidative damage in various biological systems. In this study, the shielding effect of boric acid in counteracting testicular impairment caused by glyphosate was assessed. Random allocation of male rats was performed to establish four experimental groups. Control, BA, GLY, and BA+ GLY. After the treatment phase, measurements of follicle-stimulating hormone (FSH), luteinizing hormone (LH), and testosterone were conducted to explore potential alterations in endocrine function. Testicular malondialdehyde (MDA) and glutathione (GSH) levels were examined by ELISA, while the gene expression of antioxidant enzymes-superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx)-was quantified using RT-PCR. Inflammatory cytokines including, tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β), and interleukin-10 (IL-10), were evaluated by Western blot, and Caspase-3 immunoreactivity was examined histopathologically. GLY exposure significantly increased MDA, TNF-α, and IL-1β levels while reducing IL-10, GSH, antioxidant enzyme expression, and FSH,LH, and testosterone concentrations. Co-administration of BA restored antioxidant balance, normalized hormonal levels, decreased TNF-α and IL-1β expression, elevated IL-10, and mitigated apoptosis. These results indicate that BA protects the testes from GLY-induced impairment by modulating oxidative stress, inflammation, endocrine disruption, and apoptotic cascades.

Acrylamide (ACR) is a toxic compound formed during high-temperature food processing that is known to induce oxidative stress and reproductive toxicity. This study investigated the protective effects of melatonin (MEL) on ACR-induced testicular toxicity, with a focus on hormonal regulation and steroidogenic pathways. Forty adults male Wistar rats were divided into five groups: control, ACR (50 mg/kg), ACR+MEL10 (ACR + 10 mg/kg MEL), ACR+MEL20 (ACR + 20 mg/kg MEL), and MEL20 (20 mg/kg MEL alone). Treatments were administered via intragastric gavage for 14 days. Serum follicle-stimulating hormone (FSH), luteinizing hormone (LH), and testosterone levels were measured via ELISA, alongside testicular steroidogenic enzyme levels (StAR, P450scc, 17β-HSD3). Histopathological analysis was used to assess spermatogenic integrity via Johnsen scoring. ACR exposure significantly reduced the serum FSH, LH, and testosterone levels (p< .001), with a concurrent decrease in StAR, P450scc, and 17β-HSD3 expression. Histological evaluation revealed severe spermatocyte degeneration, necrosis, and disrupted spermatogenesis. MEL administration ameliorated these effects in a dose-dependent manner. ACR+MEL10 resulted in partial restoration of hormonal and enzymatic levels (p< .05), whereas ACR+MEL20 restored these parameters to near-control levels (p> .05). MEL also mitigated histopathological damage, preserving seminiferous tubule integrity and spermatogenic function. These findings suggest that MEL exerts protective effects against ACR-induced testicular toxicity through its antioxidant and antiapoptotic effects, restoring steroidogenic enzyme activity and the hormonal balance. MEL supplementation may be a potential therapeutic strategy against environmental toxicants affecting male reproductive health. Further mechanistic studies are warranted to elucidate its full protective scope.

Lead is a highly toxic heavy metal and an environmental pollutant. Lead exposure causes damage and dysfunctions in organs. In tissues exposed to lead, ROS increase, resulting in oxidative stress, inflammation and apoptosis. In this study, we aimed to investigate the protective effects of Borago officinalis (BO) against lead, whose toxic effects are well-established. In this study, 40 Sprague-Dawley rats were used. The rats were randomly divided into 5 groups. The groups were determined as control, BO100, Pb (20 mg/kg), Pb+BO50 and Pb+BO100. After the experimental procedures were completed, the tissues were transported in cold chain and stored in -80 deep freezer until the experiments were performed. Keap-1 level was determined in spleen tissue using Western blot method. At the same time, IL-1β, IL-10, NF-ĸB, Bax, Bcl-2, Caspase-3 levels were determined by RT-PCR method. BO administration stimulated Keap-1 level in relation to oxidative stress. While BO suppressed IL-1β and NF-ĸB levels, it stimulated IL-10 level, which are anti-inflammatory markers. BO also suppressed Bax and Kaspas-3 levels, while significantly stimulating Bcl-2 level. With these effects, it was observed that BO had anti-oxidant, anti-inflammatory, anti-apoptotic effects in the spleen tissue of rats treated with lead acetate.

This study examined the antioxidant, anti-inflammatory, and neuroprotective effects of melatonin (MEL) against acrylamide (ACR)-induced neurotoxicity in Sprague-Dawley rats. The experimental groups included control, ACR, MEL10+ACR, MEL20+ACR, and MEL20. MEL at doses of 10 and 20 mg/kg, and ACR at 50 mg/kg, were administered intraperitoneally for 14 days. On the 15th day, locomotor activity was assessed, and brain tissues were analyzed biochemically, molecularly, and histopathologically. ACR exposure decreased locomotor activity, increased malondialdehyde (MDA) and reduced glutathione (GSH) levels, indicating oxidative stress, and decreased antioxidant enzyme activities (SOD, GPx, CAT). High-dose MEL (MEL20+ACR) effectively reduced lipid peroxidation and restored antioxidant enzyme activities. MEL treatment also suppressed proinflammatory cytokines (TNF-α, IL-1β, IL-6) and neuronal nitric oxide synthase (nNOS), demonstrating anti-inflammatory effects. Furthermore, MEL mitigated ACR-induced neurotoxicity by reducing acetylcholinesterase (AChE) and monoamine oxidase (MAO) levels. ER stress markers (GRP78, ATF4, ATF6, sXBP1, CHOP) and apoptotic markers (Bax, Caspase-3) were elevated following ACR exposure but were suppressed by MEL. Additionally, MEL reduced ACR-induced increases in 8-hydroxy-2-deoxyguanosine (8-OHdG) and glial fibrillary acidic protein (GFAP), markers of DNA damage and astrocyte activation, respectively. These findings underscore the potential of MEL to counteract ACR-induced neurotoxicity through its comprehensive antioxidant, anti-inflammatory, and neuroprotective actions.