Saffron (its active constituent, crocin) supplementation attenuates lipid peroxidation and protects against tissue injury.

The aim of the current study was to investigate the outcomes in a rat model of an acute swimming exercise induced oxidative stress in brain, kidney, liver, skeletal and cardiac muscles using supplementation with crocin. Rats were divided into the eight groups; Normal Control (NC: Untreated and did not swim), Crocin Control (CC: Received crocin and did not swim), Exercise-1 (E-1: Untreated and swam), Exercise-24 (E-24: Untreated and swam), Exercise-48 (E-48: Untreated and swam), Exercise+Crocin-1 (EC-1: Received crocin and swam), Exercise+Crocin-24 (EC-24: Received crocin and swam), Exercise+Crocin-48 (EC-48: Received crocin and swam). The malondialdehyde (MDA) and xanthine oxidase (XO) enzymes levels increased after swimming in untreated and crocin treated groups, but there was a lower increase in crocin treated groups. The highest MDA levels in all tissues were observed in E-1 compared to all other groups. There were significant differences between control and exercise groups in MDA levels of tissues (p < 0.001). In contrast, there were significant differences between control and exercise groups in glutathione (GSH) levels of tissues.In addition, the crocin supplementation significantly increased GSH levels and decreased MDA and XO enzyme levels when compared to untreated exercise groups. Crocin can protect the tissues against exercise induced oxidative stress by enhancing antioxidant activity (Tab. 3, Fig. 1, Ref. 37).

Protective effects of crocin on biochemistry and histopathology of experimental periodontitis in rats.

We investigated the effectiveness of crocin for preventing oxidative damage in experimentally produced periodontitis. We used three groups of 10 female Wistar rats divided into: control (C); experimental periodontitis (EP), experimental periodontitis + crocin (Cr-EP). Malondialdehyde (MDA), glutathione (GSH), total antioxidant status (TAS), total oxidant status (TOS) and superoxide dismutase (SOD) and catalase (CAT) enzyme activities were measured. We examined histopathology and inflammatory cell infiltration in gingiva and periodontal ligament. MDA and TOS levels, and SOD and CAT activities increased significantly in rats with induced periodontitis compared to the control group, while GSH and TAS levels were decreased significantly compared to the control group. Histopathologic examination revealed inflammatory cell infiltration in gingiva epithelium and subepithelial connective tissue in the EP group. Histological damage was reduced significantly after crocin treatment compared to the EP group. Crocin supplementation may help reduce oxidative damage to periodontal tissues.

Investigation of the protective effects of crocin on acrylamide induced small and large intestine damage in rats.

We investigated repair of acrylamide (AA) induced damage in intestines by administration of crocin. We used 40 male Wistar rats in four groups of 10 animals: control, AA, crocin, and AA + crocin groups. We investigated biochemical and histological changes to small and large intestine. AA ingestion decreased glutathione (GSH) levels and total antioxidant status (TAS) in the intestine compared to the control group, while superoxide dismutase (SOD) and catalase (CAT) activities, and total oxidant status (TOS) and malondialdehyde (MDA) levels were increased. Villi were shortened and villus degeneration was observed in ileum of the AA group. Degeneration of surface epithelium and Liberkühn crypts were observed in colon sections. GSH and TAS levels increased after administration of AA together with crocin, while SOD and CAT levels and TOS and MDA levels decreased; significant recovery of histological damage also was observed. We found that crocin exhibits protective effects on AA induced small and large intestine damage by inhibiting oxidative stress.

Neuroprotection against CCl4 induced brain damage with crocin in Wistar rats.

Owing to its lipophilic property, carbon tetrachloride (CCl4) is rapidly absorbed by both the liver and brain. We investigated the protective effects of crocin against brain damage caused by CCl4. Fifty rats were divided into five groups of ten: control, corn oil, crocin, CCl4 and CCl4 + crocin. CCl4 administration decreased glutathione (GSH) and total antioxidant status (TAS) levels, and catalase (CAT) activity, while significant increases were observed in malondialdehyde (MDA) and total oxidant status (TOS) levels and superoxide dismutase (SOD) activity. The cerebral cortex nuclear lamina developed a spongy appearance, neuronal degeneration was observed in the hippocampus, and heterochromatic and pyknotic neurons with increased cytoplasmic eosinophilia were observed in the hippocampus after CCl4 treatment. Because crocin exhibits strong antioxidant properties, crocin treatment increased GSH and TAS levels and CAT activities, and decreased MDA and TOS levels and SOD activity; significant improvements also were observed in histologic architecture. We found that crocin administration nearly eliminated CCl4 induced brain damage by preventing oxidative stress.

Thymoquinone is protective against 2,3,7,8-tetrachlorodibenzo-p-dioxin induced hepatotoxicity.

We investigated changes in rat liver tissues following administration of thymoquinone (TQ) against 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) induced hepatotoxicity. Fifty rats were assigned randomly to five groups of 10 as follows: control, corn oil, TCDD, TQ and TCDD + TQ. Biochemical and histopathological analyses were conducted on liver tissue. We found that 30 day TCDD administration caused histopathological changes in liver including thickening of Glisson's capsule, intracytoplasmic vacuolization in hepatocytes, sinusoidal dilation, vascular and sinusoidal congestion and inflammatory cell infiltration. TCDD administration increased malondialdehyde (MDA), total oxidant status (TOS), alanine aminotransferase (ALT), aspartate aminotransferase (AST) and alkaline phosphatase (ALP) levels in rat liver tissue and reduced glutathione (GSH), superoxide dismutase (SOD), catalase (CAT) and total antioxidant status (TAS) levels compared to all other groups. In the TQ treated group, GSH, SOD, CAT and TAS levels increased compared to all other groups. MDA, TOS, ALT, AST, ALP levels decreased compared to all other groups. Our histological findings were consistent with the biochemical findings. The oxidative and histologic effects of TCDD were eliminated by TQ treatment. TCDD administration caused oxidative stress in rat liver and TQ administered with TCDD prevented TCDD induced hepatotoxicity. TQ could be considered an alternative anti-TCDD toxicity agent.

Investigation of the effects of acrylamide applied during pregnancy on fetal brain development in rats and protective role of the vitamin E.

A liberal amount of acrylamide (AA) is produced as a result of frying or baking foods in high temperatures, and individuals take certain amounts of AA everyday by consuming these food items. Pregnant women are also exposed to AA originating from food during pregnancy and their fetus are probably affected. The rats were divided into five different groups: control (C), corn oil (CO), vitamin E (Vit E), AA, and Vit E + AA, with eight pregnant rats in each group. On the 20th day of pregnancy, fetuses were removed and brain tissues of fetuses were examined for biochemical and histological changes. AA caused degeneration in neuron structures in fetal brain tissue and caused hemorrhagic damages; dramatically decreased brain-derived neurotrophic factor levels; increased malondialdehyde, total oxidant capacity levels; and decreased reduced glutathione and total antioxidant capacity levels (p < 0.05). On the other hand, it was determined that the Vit E, a neuroprotectant and a powerful antioxidant, suppressed the effects of AA on fetal development and fetal brain tissue damage for the above-mentioned parameters (p < 0.05). It is recommended to consume food containing Vit E as a protection to minimize the toxic effects of food-oriented AA on fetus development due to the widespread nature of fast-food culture in today's life and the impossibility of protection from AA toxicity.