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.

In this study, it was aimed to investigate the protective effects of Naringin on nephrotoxicity by Cyclophosphamide (CYP)-induced rats. In our study, forty male adult Sprague Dawley rat weighing approximately 200-250 g were used and 5 gropus formed. Measurement of hematologic and biochemical parameters were done in the rat mode on the Abocus Junior Vet 5 hemogram and on Modular PP autoanalyzer instruments. In the CYP groups, Neutrophil (%) and monocyte (%) increase despite red blood cell count, white blood cell count, hematocrit value, thrombocyte count and lymphocyte (%) decrease (P<0.05). While there were a decrease in potasium and sodium levels (P<0.05), but no decrease in other parameters such as phosphorus, magnesium, chlorine and calcium. Altough glucose, creatinine and uric acid levels from renal function tests were statistically significantly increased at (P<0.05), the increase in urea, BUN and lactate dehydrogenase (LDH) values were not significant. In the histopathological exemination; It was determined that severly hydropic degeneration and coagulation necrosis in tubule ephitelia, dilatation in Bowman capsule, hyperemia in interstitial vein and glomerulus of kidney tissue by the effects of CYP. These damages in the kidney were found to be reduced as dose-dependent due to cytoprotective effects of Naringin. It was determined that different doses of Naringin suppress nephrotoxicity and the negative effect of CYP.

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.

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.