The aim of the present study was to examine the effect of monosodium glutamate (MSG) on the functions of ovary and uterus in rat. Virgin female rats of Charles Foster strain (120 gms approximately) were administrated MSG by oral gavage at a dose level of 0.8, 1.6, 2.4 gm/kgBW/day, respectively for 30 and 40 days duration. We observed a significant decrease in the duration of proestrus, estrus and metestrus phases, and increase in the duration of diestrus phase and diestrus index compared to control. We found significant increase in the levels of serum LH, FSH and estradiol in test groups of rat. We also observed significant increase in the number of primary and primordial follicles, increase in the size of graafian follicle, and decrease in the size of corpus luteum. Further, we have seen significant increase in the activities SOD, CAT and GST, decrease in the activities GR and GPx, and decrease MDA level in MSG exposed groups. These results suggest that MSG impairs the functions of the ovary probably by augmenting the release of FSH, LH and estradiol; promoting the follicular maturation and improving the biochemical mechanism for antioxidant defense. We also observed significant potentiation of the force of contraction of uterus in estrus, metestrus and diestrus phases. This result suggests that MSG potentiates the contraction of uterus probably by stimulating the estradiol sensitivity to oxytocin. From the results it is concluded that MSG suppresses the female reproductive function in rat probably by impairing the functions of ovary and uterus.

Graphical abstract

The gastrointestinal tract is directly exposed to bisphenol A (BPA)-tainted foods and beverages stored in polycarbonate plastic containers. The effect of BPA on the movement of small intestine has not been reported until now. We report here the effect of BPA on the movement of the duodenum ex vivo in a rat model. We found significant inhibition of duodenal movement by BPA (10-320 µM). We suggest that BPA-induced inhibition of duodenal movement might be due to the suppression of stimulatory and/or activation of inhibitory motor neurons in enteric plexuses innervating the longitudinal and circular visceral smooth muscle cells in the duodenal wall. We observed a significant reversal of BPA-induced depression of duodenal movement by methylene blue, a soluble guanylyl cyclase blocker and N-ω-nitro-L-arginine methyl ester, a nitric oxide (NO) synthase inhibitor; but significant potentiation of the movement by sodium nitroprusside, a NO donor. From the results, we may suggest that BPA-induced inhibition of the movement might be partially due to activation of inhibitory motor neurons that secrete NO, a relaxant, on to smooth muscle cells. Furthermore, we found significant reversal of BPA-induced depression of the movement in phentolamine, an α-adrenergic receptor blocker, pretreated preparation. This result proves that norepinephrine secreting motor neurons may also be involved in BPA-induced inhibition of the movement. From the results, we conclude that BPA inhibits the movement of the duodenum through NO-mediated soluble guanylyl cyclase and α-adrenergic signaling pathways in visceral smooth muscle cells.

The present invivo study was designed to elucidate the toxic effect of lead on oxidative stress, Na(+)K(+)ATPase and mitochondrial electron transport chain activity of the brain of Clarias batrachus. The fish were exposed to 10 and 20% of the derived 96 h LC(50) value, 37.8 and 75.6 mg L(-1), respectively, and sampled on 20, 40 and 60 days. Exposure of fish brain to lead demonstrated an increased production of reactive oxygen species, increased lipid peroxidation, loss of protein thiol groups in synaptosomal fraction with the decreased activity of Na(+)K(+)ATPase, partial inactivation of mitochondrial electron transport chain activity and energy depletion. However, no change in protein carbonyl content in synaptosomal fraction was observed due to lead exposure. Concluding the results of our investigation we suggest that lead exposure induces oxidative stress in the brain of Clarias batrachus and the decline in Na(+)K(+)ATPase activity was presumeably mediated by the combined action of lipid peroxidation and deficient mitochondrial electron transport chain activity.

Lead (Pb) is one of the most pollutant metals that accumulate in the brain mitochondria disrupting mitochondrial structure and function. Though oxidative stress mediated by reactive oxygen species remains the most accepted mechanism of Pb neurotoxicity, some reports suggest the involvement of nitric oxide (NO) and reactive nitrogen species in Pb-induced neurotoxicity. But the impact of Pb neurotoxicity on mitochondrial respiratory enzyme complexes remains unknown with no relevant report highlighting the involvement of peroxynitrite (ONOO) in it. Herein, we investigated these effects in in vivo rat model by oral application of MitoQ, a known mitochondria-specific antioxidant with ONOO scavenging activity. Interestingly, MitoQ efficiently alleviated ONOO-mediated mitochondrial complexes II, III and IV inhibition, increased mitochondrial ATP production and restored mitochondrial membrane potential. MitoQ lowered enhanced caspases 3 and 9 activities upon Pb exposure and also suppressed synaptosomal lipid peroxidation and protein oxidation accompanied by diminution of nitrite production and protein-bound 3-nitrotyrosine. To ascertain our in vivo findings on mitochondrial dysfunction, we carried out similar experiments in the presence of different antioxidants and free radical scavengers in the in vitro SHSY5Y cell line model. MitoQ provided better protection compared to mercaptoethylguanidine, N-nitro-L-arginine methyl ester and superoxide dismutase suggesting the predominant involvement of ONOO compared to NO and O. However, dimethylsulphoxide and catalase failed to provide protection signifying the noninvolvement of OH and HO in the process. The better protection provided by MitoQ in SHSY5Y cells can be attributed to the fact that MitoQ targets mitochondria whereas mercaptoethylguanidine, N-nitro-L-arginine methyl ester and superoxide dismutase are known to target mainly cytoplasm and not mitochondria. Taken together the results from the present study clearly brings out the potential of MitoQ against ONOO-induced toxicity upon Pb exposure indicating its therapeutic potential in metal toxicity.

Highlights Bisphenol A induces oxidative stress mediated liver mitochondrial damage. Bisphenol A induced damage is being protected when mitochondria are co-incubated with gallic acid. Scanning electron microscopy of mitochondrial tomography supports the biochemical observations. Gallic acid may be used as future remedial measure for the protection of bisphenol A induced damages of liver mitochondria.

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Metanil yellow (MY) is a most frequently used food color in West Bengal, India. The toxic effects of MY on the male reproductive system have been reported discriminately in animal models. The probable toxic effects of MY on female reproductive functions have not been reported till date. Therefore, this study was designed to examine the effect of MY on estrous cycle rhythmicity and ovarian folliculogenesis in female rats. Rats have been exposed to MY at three doses of 250, 500, 750 mg kgBW day for two exposure durations, 20 and 30 days. We observed significant changes in the number and duration of estrous cycle along with prominent cytoarchitectural changes in the cellular characteristics of vaginal smear of component phases of estrous cycle in a dose and duration-dependent manner in MY-treated rats compared to control rats. We also observed a significant decrease in serum follicle stimulating hormone (FSH), luteinizing hormone (LH), and estradiol levels in MY-treated rats. Further, the activities of some antioxidants enzymes in brain tissues of MY-treated rats were significantly decreased and the level of malondialdehyde (MDA), a marker of lipid peroxidation, in brain tissues of MY-treated rats was also significantly increased. The ovarian folliculogenesis in this study was also significantly impaired in MY-treated rats. In conclusion, MY impairs the estrous cycle and ovarian folliculogenesis in female rats by inhibiting the secretion of FSH and estradiol from the ovary, and inducing the oxidative stress in hypothalamic-pituitary-gonadal axis. © 2015 Wiley Periodicals, Inc. Environ Toxicol 31: 2057-2067, 2016.