Protective role of vitamin E against acrylamide-induced testicular toxicity from pregnancy to adulthood: insights into oxidative stress and aromatase regulation.

Acrylamide (ACR) is a toxic chemical frequently encountered in daily life, posing health risks. This study aimed to elucidate the molecular-level mechanism of ACR's toxic effects on testicles and investigate whether Vitamin E can mitigate these effects. A total of 40 adult pregnant rats were utilized, divided into four groups: Control, ACR, Vitamin E, and ACR + Vitamin E. ACR and Vitamin E were administered to the mother rats during pregnancy and lactation, and to the male offspring until the 8th week post-birth. Serum hormone levels, oxidant-antioxidant parameters, histopathological examination of testicular tissue, and mRNA and protein levels of the testicular and liver aromatase gene were analyzed. Spermiogram analysis was conducted on the collected sperm samples from the male offspring. The results revealed that ACR exposure adversely affected hormone levels, oxidant-antioxidant parameters, histological findings, as well as aromatase gene and protein expressions. However, Vitamin E administration effectively prevented the toxic effects of ACR. These findings demonstrate that ACR application significantly impairs the reproductive performance of male offspring rats by increasing liver aromatase activity.

Biochemical and histopathological investigation of the protective effects of melatonin and vitamin E against the damage caused by acetamiprid in Balb-c mouse testicles at light and electron microscopic level.

The protective effects of melatonin (Mel) and vitamin E (Vit E) against the negative effects of acetamiprid (Acmp) on testicles, reproductive hormones, and oxidative stress parameters were investigated in the present study. A total of 50 Balb-c male mice were used in 7 groups; 6 mice in the control groups (distilled water, corn oil, ethanol), and 8 in other groups (Acmp, Acmp + Mel, Acmp + Vit E, Acmp + Vit E + Mel). After the experiment, which lasted 21 days, hematoxylin eosin (H&E), periodic acid Schiff (PAS), and caspase-3 immunohistochemical (IHC) staining was performed on the testicular tissues. Also, the tissues were examined ultrastructurally with the transmission electron microscopy (TEM). In the Acmp group, there were decreased seminiferous tubule diameter and epithelial thickness, epithelial degeneration, decreased spermatozoa in the lumen, decreased PAS-positive staining in the seminiferous epithelial basement membrane, edema in the interstitial area, and hydropic degeneration in Leydig cells. Caspase-3 immunoreactivity was higher than in the other groups. TEM examination showed degeneration in tubule cells, lysosomal accumulation in cells of the spermatogenic line, vacuolizations with myelin figures, and necrosis. Hydropic degeneration, electron-dense lipid vacuoles, and chromatolysis were evident in the Leydig cell cytoplasm. In Sertoli cells, electron-dense lysosomal deposits were noted. In biochemical terms, there were decreased tissue glutathione (GSH) and total antioxidant status (TAS), and increased malondialdehyde (MDA) and total oxidant status (TOS). Plasma luteinizing hormone (LH), follicular stimulating hormone (FSH), and testosterone levels were decreased. In the groups with melatonin, vitamin E, and both were applied together, tissue damage, and apoptotic cell death were reduced at both light microscopic and ultrastructural levels. In biochemical terms, there were decreased oxidative parameters and increased hormonal parameters. It was found that vitamin E was more effective in decreasing oxidative parameters and increasing antioxidative parameters when compared to melatonin, and hormonal parameters increased at a higher level in the Acmp + Vit E group than in all groups. As a result, it was found that exposure to Acmp caused damage to testicular tissue, induced oxidative stress in testicles, and decreased plasma LH, FSH, and testosterone levels, and although vitamin E is more effective than melatonin in preventing this damage, both are effective.

Comparison of the efficacies of polycaprolactone filler and lidocaine-added filler on neocollagenesis in a rat model.

BACKGROUND: Polycaprolactone (PCL) is a semi-permanent filler stimulating neocollagenesis. Lidocaine is frequently used to reduce the pain and, however, may have negative effects on collagen. It was aimed to compare the histological changes on rat skin and efficacies of PCL filler and lidocaine addition. OBJECTIVE: In this study, results of PCL and PCL+Lidocaine application on rat skin were compared using hematoxylin-eosin (H&E) staining, Masson's trichrome (MT) staining, and electron microscope (EM). METHODS: A total of 30 adult female rats were divided into three groups: the control group, the PCL group, and the PCL+Lidocaine group. The tissue samples taken at months 2 and 4 were examined using H&E, MT, and EM. RESULTS: At month 2, dermis thickness, fibroblast count, and collagen fiber diameter increased similarly in the PCL and PCL+Lidocaine groups. Collagen fiber diameter was significantly higher in the PCL group than in the PCL+Lidocaine (p:0.016) and control groups (p:0.009). At month 4, no significant difference was detected between the PCL and PCL+Lidocaine groups in terms of fibroblast count, collagen fiber count, and collagen fiber diameter; dermis thickness was lower in the PCL+Lidocaine group at month 4 (p < 0.46). Dermis thickness, fibroblast count, collagen fiber count, and collagen fiber diameter were found to be significantly lower than in the PCL and PCL+Lidocaine groups. CONCLUSIONS: Our study showed that lidocaine addition to PCL filler does not affect the efficacy of the filler and PCL filler stimulates neocollagenesis.

Crocin attenuates oxidative and inflammatory stress-related periodontitis in cardiac tissues in rats.

BACKGROUND: Periodontitis, a chronic inflammatory disease affecting the supporting tissues around the teeth, causes significant inflammatory and oxidative changes in cardiac tissue. Crocin is the active constituent of Crocus sativus (saffron) which has antioxidant properties and is protective against cardiovascular disturbances. OBJECTIVES: The present study aimed to investigate the protective effects of crocin on periodontitis-induced oxidative/inflammatory cardiac degeneration in rats in vivo. MATERIAL AND METHODS: Thirty female Sprague Dawley rats were randomly divided into 3 groups: control group, periodontitis group (PD) and periodonditis plus crocin group (PD+Cr). Experimental periodontitis was induced by placing silk ligatures on the maxillary second molar teeth for 30 days. Afterward, crocin (100 mg/kg body weight/day) was administered to the PD+Cr group and saline was administered to the PD group and the control group for 15 days. The subjects were sacrificed on the 45th day. RESULTS: Histological and biochemical analyses demonstrated that inducing periodontitis caused obvious damage to cardiac tissues which was significantly ameliorated by crocin (p < 0.05). Significant improvements in bone resorption parameters (cross-linked C-telopeptide of type I collagen and bone alkaline phosphatase) were also observed in the PD+Cr group (p < 0.05). In addition, crocin caused significant reductions of malondialdehyde levels and total oxidant score while antioxidant levels (glutathione, superoxide dismutase, total antioxidant score, and catalase) were significantly higher in PD+Cr group (p < 0.05). CONCLUSIONS: This study reveals that periodontitis may cause oxidative damage in cardiac tissue and crocin improves periodontitis-induced degenerative changes in heart tissue, which is associated with its antioxidant properties.

A light microscopic investigation of the renoprotective effects of α-lipoic acid and α-tocopherol in an experimental diabetic rat model.

We investigated the effects of α-lipoic acid (AL) and α-tocopherol (AT) on renal histopathology in a streptozotocin (STZ) induced diabetic rat model. Adult male rats were divided into six groups: group 1, saline only; group 2, AL only; group 3, AT only; group 4, STZ only; group 5, STZ + AL; group 6 STZ + AT. Experimental diabetes was induced by STZ. AL and AT were administered for 15 days. Kidney sections were examined using a light microscope after hematoxylin and eosin (H & E), periodic acid-Schiff (PAS) and caspase-3 staining. Histological damage to glomeruli, tubule epithelial cells and basement membrane was observed in group 4. Administration of AT and AL reduced renal injury in the diabetic rats. Group 5 exhibited a greater curative effect on diabetic rats than group 6. AT and AL may be useful for preventing diabetic renal damage.

Protective effects of melatonin and vitamin E in acetamiprid-induced nephrotoxicity.

Investigation of probable toxic effects of acetamiprid (ACMP) on kidney and comparative analysis of the probable protective effects of vitamin E and melatonin were conducted in the present study. The ethics committee approval was obtained from Inonu University Medical Faculty Ethics Committee. Fifty Balb-c mice were randomly assigned to control, corn oil, ethyl alcohol, ACMP, ACMP + melatonin, ACMP + vitamin E, and ACMP + melatonin + vitamin E groups. At the end of the experiments, rat kidney tissues were incised under anesthesia. Blood samples and kidney tissues were examined. After 21 days of ACMP administration, it was observed that malondialdehyde (MDA), total oxidant status (TOS), BUN, creatinine, IL-6, IL-1ß, and TNF-α levels, histopathological damage, and Caspase-3 immunoreactivity scores increased, and glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), and total antioxidant status (TAS) levels decreased, and histopathological damages were observed. Melatonin and vitamin E administration led to improvements in oxidative stress parameters, renal functions, inflammatory markers, and histopathological findings. ACMP administration led to nephrotoxicity in rat kidney tissues. Although melatonin and vitamin E administrations were effective on ACMP nephrotoxicity separately, co-administration of both was quite effective. Concomitant use of melatonin and vitamin E could be effective on prevention of toxicity.

Protective effect of crocin on food azo dye tartrazine-induced hepatic damage by improving biochemical parameters and oxidative stress biomarkers in rats.

The objective of the present study was to demonstrate the protective effect of crocin on the adverse effects of tartrazine on liver. Crocin is a carotenoid and a strong free radical scavenger. Forty rats were randomly divided into 4 groups (n = 10). The first group was the control group (C) and saline solution was administered to this group. The second group (Cr) was administered 50 mg/kg crocin. The third group (T) was administered 500 mg/kg tartrazine. The fourth group (T+Cr) was administered the same doses of both crocin and tartrazine as the previous groups for 21 days. It was determined that tartrazine increased liver superoxide dismutase (SOD) activity, malondialdehyde (MDA) and total oxidant status (TOS) levels and catalase (CAT) activity, decreased glutathione (GSH), and total antioxidant status (TAS) levels. Furthermore, tartrazine administration resulted in significant increases in plasma aspartate aminotransferase (AST), alanine aminotransferase (ALT) and alkaline phosphatase (ALP) activities and pathological changes in the liver. When tartrazine administered rats were treated with crocin for 21 days, the biochemical parameters improved, and liver tissues were restored. Thus, it was demonstrated that crocin had protective effects on the adverse effects caused by tartrazine administration.

The protective role of crocin in tartrazine induced nephrotoxicity in Wistar rats.

The present study was conducted to investigate the changes in rat kidney tissues after administration of tartrazine (T) and crocine (Cr). The latter was applied for its protective properties. The present study was conducted with the approval of Inonu University, Faculty of Medicine, Experimental Animals Ethics Committee. Forty rats were randomly divided into 4 equal groups (Control, T, Cr, T + Cr). At the end of the experiment, the rats were decapitated. Biochemical and histopathological studies were conducted on excised rat kidney tissues. It was determined that there was a significant increase in MDA, TOS, SOD, CAT, Bun, Creatinine levels in tartrazine administered rat kidney tissues for 21 days, while GSH and TAS levels decreased (P ≤ 0.05) when compared to all other groups. On the other hand, it was identified that Cr administration statistically significantly increased GSH and TAS levels in rat kidney tissues when compared to all other groups and decreased MDA and TOS levels to control group levels (P < 0.05). T group kidney sections exhibited different degrees of collapse in the glomeruli. In most sections, different levels of inflammatory cell infiltration and vascular and capillary congestion were detected in peritubular interstitial tissue. It was determined that T leads to adverse effects on rat kidney tissues. Administration of Cr + T prevented T induced nephrotoxicity. Thus, it was concluded that Cr could be utilized as a new type of anti-tartrazine toxicity agent.

Does omega-3 have a protective effect on the rat adrenal gland exposed to 900 MHz electromagnetic fields?

The aim of this study was to investigate the harmful effects of exposure to 900-megahertz (MHz) electromagnetic fields (EMF) and the protective effects of omega-3 (Omg-3) against EMF in the rat adrenal gland. Eighteen Wistar albino rats were randomly assigned into three groups, control (Cont), EMF, and EMF + Omg-3. The EMF and EMF + Omg-3 groups both consisted of six rats exposed to an EMF of 900 MHz for 60 min/day for 15 days. No procedure was applied to the six rats in the Cont group. At the end of the experiment, all rats were sacrificed, and the mean volumes of the cortex and medulla of the adrenal gland were estimated using a stereological counting technique. The stereological results showed that the mean volume of the adrenal gland increased significantly in the EMF-exposed groups compared to the Cont group. Additionally, the mean volume of the adrenal gland was significantly lower in the EMF + Omg-3 group compared to the EMF group. We suggest that Omg-3 therapy aimed at suppressing the effects of EMF may prove a safe alternative for animals, whether or not they are exposed to EMF.