Sentence examples for life cycle exposure from inspiring English sources

The results showed for the first time, a life cycle exposure to MC-LR caused growth inhibition, decreased ovary weight and ovarian ultra-pathological lesions.

The results, for the first time, show a life cycle exposure to MC-LR causes growth inhibition, testicular damage and delayed sperm maturation.

Our findings indicated that a life cycle exposure to MC-LR causes endocrine disruption with organic and functional damage of the testis, which might compromise the quality of life for the survivors and pose a potent threat on fish reproduction and thus population dynamics in MCs-contaminated aquatic environments.

Our findings indicate that a life cycle exposure to MC-LR impairs the development and reproduction of female zebrafish by disrupting the transcription of related HPGL-axis genes, suggesting that MC-LR has potential adverse effects on fish reproduction and thus population dynamics in MCs-contaminated aquatic environment.

It has also been shown that life cycle exposure of fathead minnow to an inordinately low concentration of EE2 (0.32 ng/L) was sufficient to decrease the egg fertilisation and to skew the sex ratios towards female[ 8].

Similarly, life cycle exposure of fathead minnow and zebrafish to ethinyl-estradiol at concentrations of 4 and 3 ng/L, respectively, results in a 100% inhibition of reproduction; but in fathead minnow this effect is caused by a complete feminization of the gonads (Länge et al. 2001), whereas in zebrafish it seems to be caused by arrested testicular development (Fenske et al. 2004).

Life-cycle exposure to MC-LR caused delayed ovarian maturation and sperm development along with ultrapathological lesions in the brain and liver.

The purpose of this study was to characterize the thyroid endocrine disruption induced by life-cycle exposure to BDE-47 in adults and offspring of zebrafish (Danio rerio).

Here we use DEB theory and explicitly a recently developed version of the DEBtox model [ 17, 19], to investigate the physiological mode of action of three different types of chemical stressors (the metal cadmium, the non-polar organic fluoranthene, and the herbicide atrazine) during a whole life-cycle exposure of the nematode Caenorhabditis elegans.

In the F1 generation (after full life-cycle exposure, 314 dpf), 284 adults from six replicate tanks in each of the remaining exposure groups (0.5 ng/L and 5 ng/L EE2 treatments with no F1 exposure; 0.5 and 5 ng/L EE2 and 5 ng/L E2 treatments with exposure stopped at 75 dpf in F 1 ) were weighed; we then collected blood samples and determined the hematocrit value.

Even though some PPCPs are extremely persistent and introduced to the environment in very high quantities and perhaps have already gained ubiquity worldwide, others could act as if they were persistent, simply because their continual infusion into the aquatic environment serves to sustain perpetual life-cycle exposures for aquatic organisms.