Glyphosate is the most popular herbicide used worldwide. This study aimed to investigate the adverse effects of glyphosate on the small intestine and gut microbiota in rats. The rats were gavaged with 0, 5, 50, and 500 mg/kg of body weight glyphosate for 35 continuous days. The different segments of the small intestine were sampled to measure indicators of oxidative stress, ion concentrations and inflammatory responses, and fresh feces were collected for microbiota analysis. The results showed that glyphosate exposure decreased the ratio of villus height to crypt depth in the duodenum and jejunum. Decreased activity of antioxidant enzymes (T-SOD, GSH, GSH-Px) and elevated MDA content were observed in different segments of the small intestine. Furthermore, the concentrations of Fe, Cu, Zn and Mg were significantly decreased or increased. In addition, the mRNA expression levels of IL-1β, IL-6, TNF-α, MAPK3, NF-κB, and Caspase-3 were increased after glyphosate exposure. The 16 S rRNA gene sequencing results indicated that glyphosate exposure significantly increased α-diversity and altered bacterial composition. Glyphosate exposure significantly decreased the relative abundance of the phylum Firmicutes and the genus Lactobacillus, but several potentially pathogenic bacteria were enriched. In conclusion, this study provides important insight to reveal the negative influence of glyphosate exposure on the small intestine, and the altered microbial composition may play a vital role in the process.

Rice (Oryza sativa L.) grown on Zn mine waste contaminated soils has caused unequivocal Cd effects on kidney and occasional bone disease (itai-itai) in subsistence rice farmers, but high intake of Cd from other foods has not caused similar effects. Research has clarified two important topics about how Cd from mine waste contaminated rice soils has caused Cd disease: (1) bioaccumulation of soil Cd into rice grain without corresponding increase in Zn, and (2) subsistence rice diets potentiate Cd absorption/bioavailability and risk to farm families. Absorption of Cd by rice roots occurs on the NRAMP5 Mn²⁺ transporter. Although other transporters can influence Cd uptake-transport to shoots and grain, making NRAMP5 null greatly reduces grain Cd. Zn²⁺ has little ability to inhibit Cd²⁺ transfer in rice but clearly inhibits Cd uptake in other plant species. The bioavailability of dietary Cd is increased for subsistence rice diets. Research has identified that low levels and bioavailability of Zn and Fe in polished rice grain cause upregulation of Cd absorption on the Fe²⁺ transporter of duodenum cells (DMT1). Added dietary Zn can also inhibit intestinal Cd absorption somewhat. Nutritional stress (Fe, Zn deficiency) in humans consuming subsistence rice diets thus promotes Cd accumulation and adverse effects. No other dietary (crop) Cd exposure has caused unequivocal Cd-induced renal proximal tubular dysfunction (the first adverse Cd effect) in humans. Recognition of the very unusual nature of Cd risk from rice compared to other crops should be taken into account in setting international limits of Cd in rice and other foods.

Bisphenol S, an industrial chemical, has raised concerns for both human and ecosystem health. Yet, health hazards posed by bisphenol S (BPS) exposure remain poorly studied. Compared to all tissues, the intestine and the liver are among the most affected by environmental endocrine disruptors. The aim of this study was to investigate the molecular effect of BPS on gene expression implicated in the control of glucose metabolism in the intestine (apelin and its receptor APJ, SGLT1, GLUT2) and in the liver (glycogenolysis and/or gluconeogenesis key enzymes (glucose-6-phosphatase (G6Pase) and phosphoenolpyruvate carboxykinase (PEPCK)) and pro-inflammatory cytokine expression (TNF-α and IL-1β)). BPS at 25, 50, and 100 μg/kg was administered to mice in water drink for 10 weeks. In the duodenum, BPS exposure reduces significantly mRNA expression of sodium glucose transporter 1 (SGLT1), glucose transporter 2 (GLUT2), apelin, and APJ mRNA. In the liver, BPS exposure increases the expression of G6Pase and PEPCK, but does not affect pro-inflammatory markers. These data suggest that alteration of apelinergic system and glucose transporters expression could contribute to a disruption of intestinal glucose absorption, and that BPS stimulates glycogenolysis and/or gluconeogenesis in the liver. Collectively, we reveal that BPS heightens the risk of metabolic syndrome.

Glyphosate is the active component of several commercial formulations as in Roundup®. The present study was investigated the toxic effects of pure glyphosate or Roundup® on the liver and small intestine of chick embryos. On day 6, a total of 180 fertile eggs injected with deionized water (control group), 10 mg pure glyphosate, or 10 mg of the active ingredient glyphosate in Roundup®/kg egg mass. The results showed an increase in relative weights of the liver in embryos that treated with Roundup®. Furthermore, oxidative stress was observed in the embryos treated with glyphosate or Roundup®, increased total superoxide dismutase, and content of malondialdehyde in the liver and intestine; moreover, decrease of glutathione peroxidase in the liver with increased in the intestine compared with the control. Besides, glutamic-pyruvic transaminase was increased in Roundup® group compared with other groups. Moreover, histopathological alterations in the liver and intestine tissues were observed in treated groups. Suppression of hepatic CYP1A2, CYP1A4, CYP1B1, and MDR1 mRNA expression after exposed to Roundup®. Furthermore, inhibition of CYP1A4 in the duodenum, CYP1A4, and MRP2 in the jejunum in embryos exposed to glyphosate or Roundup®. In addition, glyphosate treatment caused an increase of CYP3A5, CYP1C1, and IFNY mRNA expression in the jejunum and CYP1A2 expression in the ileum, while IFN-Y gene increase in embryos treated with Roundup®. In conclusion, in ovo exposure to glyphosate caused histopathological alterations and induced oxidative stress in the liver and small intestines. Moreover, the expression of cytochrome P450, MDR1, and MRP2 transporters was also modulated in the liver and small intestines for chick embryos.

The comparative anticoccidial effects of herbal products with a standard synthetic anticoccidial drug on the production performance, intestinal histology, and some blood biochemical parameters in broilers exposed to experimental coccidiosis was investigated. One-day-old broiler chicks (n = 336) were randomly distributed into six groups. One group served as a control, the second was treated with the coccidial infection, the third was treated with synthetic anticoccidial drug (Elancoban), the fourth group was treated with an herbal product (Cozante), the fifth group of birds was treated with Norponin, and the sixth group was treated with Emanox. The results indicated that BWG, BW, FCR, and PEF decreased significantly (P < 0.05) in the positive control. Body weight gain, BW, and PEF were significantly (P < 0.01) high in Elancoban-treated birds. On day 25, lesion score was significantly (P < 0.01) low in duodenum, jejunum, and ceca in Elancoban-treated birds control. On day 30, lesion score was significantly (P < 0.05) low in Emanox-treated birds as compared with the positive control. Albumin concentration was significantly (P < 0.01) low in Emanox while glucose concentration was significantly (P < 0.01) high in all the treated groups compared with the positive control birds. The total antioxidant capacity was significantly (P < 0.05) high in Emanox on day 15 and 30 as compared with the positive control. The results showed that birds exposed to the natural anticoccidial products showed improved villi and total antioxidant capacity. We concluded that herbal products performed better than the positive control group.