Zahra Goodarzi

Co-exposure to noise and nanomaterials, such as silver nanoparticles (Silver-NPs), is a common occurrence in today’s industries. This study aimed to investigate the effects of exposure to noise and the administration of silver-NPs on the liver tissue of rats. Thirty-six adult male albino Wistar rats were randomly divided into six groups: a control group (administered saline intraperitoneally), two groups administered different doses of Silver-NPs (50 mg/kg and 100 mg/kg, 5 days a week for 28 days), two groups exposed to noise in addition to Silver-NPs (at the same doses as mentioned before), and a group exposed only to noise (104 dB, 6 hours a day, 5 days a week for 4 weeks). Blood samples were taken to assess hepatic-functional alterations, such as serum ALP, ALT, and AST levels. Additionally, biochemical parameters (MDA, GPX, and CAT) and the silver concentration in the liver were measured. Histopathological analysis, mRNA expression (P53 and NF-κB), protein expression (CYP450), and liver weight changes in rats were also documented. The study found that the administration of Silver-NPs and exposure to noise resulted in elevated levels of ALP, ALT, AST, and MDA ( p < .01). Conversely, GPX and CAT levels decreased in all groups compared with the control group ( p < .0001). There was a significant increase ( p < .05) in liver weight and silver concentration in the liver tissues of groups administered Silver-NPs (50 mg/kg) plus noise exposure, Silver-NPs (100 mg/kg), and Silver-NPs (100 mg/kg) plus noise exposure, respectively. The expression rate of P53, NF-κB, and cytochromes P450 (CYPs-450) was increased in the experimental groups ( p < .05). These findings were further confirmed by histopathological changes. In conclusion, this study demonstrated that exposure to noise and the administration of Silver-NPs exacerbated liver damage by increasing protein and gene expression, causing hepatic necrosis, altering biochemical parameters, and affecting liver weight.

Background: This research aimed to evaluate the protective effects of Artemisia Absinthium L . (Abs) against liver damage induced by aluminium oxide nanoparticles (Al ₂ O ₃ NPs) in rats, including both structural and functional changes associated with hepatotoxicity. Methods: Thirty-six rats were randomly divided into six groups ( n = 6). The first group received no treatment. The second group was orally administered Abs at a dose of 200 mg/kg/b.w. The third and fifth groups were injected intraperitoneally with γ-Al ₂ O ₃ NPs and α-Al ₂ O ₃ NPs, respectively, at a dose of 30 mg/kg/b.w. The fourth and sixth groups were pre-treated with oral Abs at a dose of 200 mg/kg/b.w. along with intraperitoneal injection of γ-Al ₂ O ₃ NPs and α-Al ₂ O ₃ NPs, respectively, at a dose of 30 mg/kg/b.w. Results: Treatment with γ-Al ₂ O ₃ NPs resulted in a significant decrease ( P < 0.05) in total body weight gain, relative liver weight to body weight, and liver weight in rats. However, co-administration of γ-Al ₂ O ₃ NPs with Abs significantly increased body weight gain ( P < 0.05). Rats treated with Al ₂ O ₃ NPs (γ and α) exhibited elevated levels of malondialdehyde (MDA), inducible nitric oxide synthase (iNOS), alanine transaminase (ALT), and aspartate aminotransferase (AST). Conversely, treatment significantly reduced glutathione peroxidase (GPx), catalase (CAT), total superoxide dismutase (T-SOD), and total antioxidant capacity (TAC) levels compared to the control group. Furthermore, the expression of heme oxygenase-1 (HO-1) and metallothionein-1 (MT-1) mRNAs, cytochrome P450 (CYP P450) protein, and histopathological changes were significantly up-regulated in rats injected with Al ₂ O ₃ NPs. Pre-treatment with Abs significantly reduced MDA, AST, HO-1, and CYP P450 levels in the liver, while increasing GPx and T-SOD levels compared to rats treated with Al ₂ O ₃ NPs. Conclusion: The results indicate that Abs has potential protective effects against oxidative stress, up-regulation of oxidative-related genes and proteins, and histopathological alterations induced by Al ₂ O ₃ NPs. Notably, γ-Al ₂ O ₃ NPs exhibited greater hepatotoxicity than α-Al ₂ O ₃ NPs.

Cadmium contributes to nephrotoxicity linked with oxidative stress in humans and animals. This study used Atorvastatin to examine its effect on cadmium chloride-induced nephrotoxicity in a rat model using biochemical and histological methodologies. Experiments were performed on 56 adult male Wistar rats (200 ± 20 g), randomly assigned to eight groups. Rats in Group A received physiologic saline. Group B was treated with a dosage of 20 mg/ kg body weight/day AT for 15 days. Groups C, D, and E received CdCl2 with dosages of 1, 2, and 3 mg/kg body weight, respectively. Groups F, G, and H were pretreated with Atorvastatin, 30 min prior to the administration of CdCl2. Rats received intra-gastric Atorvastatin for 15 days during which cadmium chloride was given from days 8 to 15. On day 16, blood samples were collected, and kidneys were excised to evaluate the biochemical and histopathological changes. Cadmium chloride significantly increased malondialdehyde (MDA), serum creatinine (Cr), blood urea nitrogen (BUN), and decreased superoxide dismutase (SOD), glutathione (GSH), and glutathione peroxidase (GPx) levels. Administration of Atorvastatin (20 mg/kg) significantly decreased lipid peroxidation, BUN and Cr, while it significantly increased glutathione and antioxidant enzymes activity. Atorvastatin improved the histological changes and all biochemical markers and shed light on its protecting role against cadmium chloride-induced oxidative stress in the kidney. GRAPHICAL ABSTRACT

Simvastatin attenuates chromium-induced nephrotoxicity in rats

Background: Chromium is a naturally occurring heavy metal found in the environment. Objectives: The aim of the present study was to determine the effect of simvastatin (SIMV) on sodium dichromate [Cr(VI)]-induced oxidative stress in the rat lung. Materials and Methods: Forty-eight adult male Wistar rats (180 - 220 g weight) were randomly assigned to eight groups (each n = 6). Group one received SIMV 20 mg/kg/day. Group two was given vehicle only. Groups three, five, and seven received intraperitoneal (i.p.) Cr(VI) at doses of 8, 12, and 16 mg/kg body weight, respectively, for eight consecutive days. Groups four, six, and eight were pretreated with 20 mg/kg SIMV 30 minutes prior to administration of Cr(VI) at doses of 8, 12, and 16 mg/kg, respectively, for eight consecutive days. Twenty-four hours after the last administration, the animals were killed with an overdose of sodium pentobarbital. Lung tissues were excised for measurements of malondialdehyde (MDA) and glutathione (GSH), and for histopathological examination. Results: The level of GSH was significantly decreased in the Cr(VI)-treated rats. In contrast, the lung level of MDA was significantly increased in a dose-dependent manner in the Cr(VI)-treated rats when compared to the control animals. SIMV had no effect on GSH and MDA levels compared to the control rats, but there were significantly increased GSH concentrations and decreased MDA levels in lungs of rats treated with Cr(VI). Conclusions: The observations suggest that SIMV may have a protective effect against Cr(VI)-induced oxidative stress in the rat lung. Keywords: Simvastatin; Sodium Dichromate; Malondialdehyde; Glutathione; Rat

The aim of the present study is to determine the effect of Chloramphenicol (CAP) on rat liver and small intestine. Effect of phenobarbital (PB) on CAP toxicity was also investigated. Rats were received CAP at doses of 0, 200, 400 and 600 mg/kg. Another group was pretreated with 80 mg/kg PB 30 min prior to administration of various doses of CAP. The experiment was repeated for seven consecutive days. Blood was collected for determination of serum aspartate aminotransferase (AST) alanine aminotransferase (ALT). The liver and small intestine tissues were processed for light microscopy. CAP induced a dose dependent elevation of AST and ALT and produced injury in the liver and small intestine when compared to control animals. PB markedly decreased AST and ALT levels and protected liver and small intestine against CAP-induced toxicity. Conclusion : This study suggested rat liver and small intestine have potential to bioactivate CAP.