Characterizing titanium dioxide and zinc oxide nanoparticles in sunscreen spray.

OBJECTIVE: Numerous commercial products contain titanium dioxide (TiO2 ) and zinc oxide (ZnO) nanoparticles (NPs); however, many of these are not labelled as containing NPs. This study sought to develop an effective means of characterizing TiO2 and ZnO NPs in sunscreen sprays, including the size, shape and composition of the particles as well as their aggregation/agglomeration characteristics. METHODS: Transmission electron microscopy (TEM) coupled with a window-type microchip K-kit/copper grid and X-ray diffraction (XRD) was used to characterize the oxide NPs. RESULTS: TME pre-treatment was performed using two approaches: using a conventional copper grid (requiring dilution) and using a K-kit (not requiring dilution). The use of K-kit in conjunction with XRD makes it possible to obtain direct measurements from samples that have not undergone pre-treatment, which could otherwise alter the nature of the samples, such as the degree of agglomeration. XRD was used to obtain information related to particle size and crystal structure. A strong correlation was observed between XRD and TEM measurements. CONCLUSION: The proposed measurement methods were shown to be highly effective in the characterization of oxide NPs in sunscreen sprays, providing consistent information related to NPs and their interactions in the formulations.

LncRNA colon cancer-associated transcript 1 (CCAT1) promotes proliferation and metastasis of ovarian cancer via miR-1290.

OBJECTIVE: Ovarian cancer is one of the leading causes of cancer-related death in women, but treatment remained unsatisfactory. Studies have shown that lncRNA colon cancer-associated transcript 1 (CCAT1) plays an important regulatory role in different cancers, but its role in ovarian cancer remained largely unclear. PATIENTS AND METHODS: Quantitative Real-time polymerase chain reaction (qRT-PCR) was applied to detect the expression of lncRNA CCAT1 in ovarian cancer and adjacent tissue, and analysis was applied to explore the relationship between expression and clinical characteristic. After lncRNA CCAT1 suppression, Cell Counting Kit-8 (CCK8) and wound-healing assay were used to detect the proliferation and metastasis ability of ovarian cancer, respectively. RESULTS: qRT-PCR showed that lncRNA CCAT1 was highly expressed in ovarian cancer tissue, compared with adjacent tissue. Moreover, we found that the expression of lncRNA CCAT1 was closely related to prognosis, tumor size, and lymph node metastasis. We also found that lncRNA CCAT1 could sponge miR-1290 in ovarian cancer. CONCLUSIONS: In this study, we found that lncRNA CCAT1 could sponge miR-1290 in ovarian cancer, and was closely related to prognosis, proliferation, and metastasis.

Characterization of titanium dioxide and zinc oxide nanoparticles in sunscreen powder by comparing different measurement methods.

Numerous consumer products, such as cosmetics, contain nanoparticles (NPs) of titanium dioxide (TiO2) or zinc oxide (ZnO); however, this raises questions concerning the safety of such additives. Most of these products do not indicate whether the product includes NPs. In this study, we characterized metal oxide NPs according to size, shape, and composition as well as their aggregation/agglomeration characteristics. In order to comprehend quickly the characterization of metal oxide NPs, we employed single particle inductively coupled plasma (SP-ICPMS) to help quantify the size of metal oxide NPs; then, we use transmission electron microscopy (TEM) to corroborate the results. The crystal size and structure was measured by X-ray diffraction (XRD), there are two crystal phase of TiO2 NPs in sunscreen powder showed in XRD. However, SP-ICPMS proved highly effective in determining the size of NPs, the results of which remarkably good agreement with the TEM measurements. Pre-treatment included a conventional copper grid (requiring sample dilution) to evaluate the size, shape and composition of primary particles or plastic embedding (without the need for sample dilution) to evaluate the aggregate/aggregation of native NOAAs. The proposed method is an effective and fast approach to the characterization of oxide NPs in cosmetic sunscreen powder. These findings outline an alternative approach to the analysis of NPs in powder-form matrix.

[Impact of maternal risky behaviors on the behaviors of children born to adolescent and young mothers].

Objective: To examine the impact of maternal risky behaviors on the behaviors of children born to adolescent and young mothers. Methods: Adolescents and young Chinese mothers were recruited from an integrated young mother supportive program in Hong Kong between January and June 2015. Eligible mothers were asked to complete a questionnaire on their sociodemographic characteristics and history of risky behavior as well as their children's behaviors. Multiple regression analyses were conducted to explore the association between maternal risky behaviors and their children's behaviors. Results: Among 201 respondents, there were 187 (93.0%) ex-drinkers, 136 (67.7%) ex-smokers, and 83 (41.3%) ex-addicts. Compared to the reference group, children of mothers with drug use behaviors were more likely to have abnormal SDQ total difficulties scores (odds ratio 2.60, P=0.01), those of ex-drinking mothers had more behavioral difficulties and more conduct problems (B=3.82 and 1.37, P both=0.01) and those of ex-smoking mothers had more conduct problems (B=0.74, P=0.01) after adjustment for confounders. Children of active drug-taking mothers also had more emotional symptoms (B=1.77, P=0.04) and hyperactivity/inattention problems (B=2.14, P=0.03). Conclusion: The history of mother's risky behavior was significantly associated with the behavioral problems of the children.

Dopamine decreases expression of type-1 angiotensin II receptors in renal proximal tubule.

Systemic and/or locally produced angiotensin II stimulates salt and water reabsorption in the renal proximal tubule. In vivo, dopamine (DA) may serve as a counterregulatory hormone to angiotensin II's acute actions on the proximal tubule. We examined whether dopamine modulates AT1 receptor expression in cultured proximal tubule cells (RPTC) expressing DA1 receptors. Dopamine decreased basal RPTC AT1 receptor mRNA levels by 67 +/- 7% (n = 10; P < 0.005) and decreased 125I-angiotensin II binding by 41 +/- 7% (n = 4; P < 0.05). The DA1-specific agonist, SKF38393 decreased basal AT1 receptor mRNA levels (65 +/- 5% inhibition; n = 5; P < 0.025), and the DA1-specific antagonist, SCH23390 reversed dopamine's inhibition of AT1 receptor mRNA expression (24 +/- 10% inhibition; n = 8; NS) and angiotensin II binding (5 +/- 15%; n = 4; NS). DA2-specific antagonists were ineffective. In rats given L-DOPA in the drinking water for 5 d, there were decreases in both proximal tubule AT1 receptor mRNA expression (80 +/- 5%; n = 6; P < 0.005) and specific [125I] Ang II binding (control: 0.74 +/- 0.13 fmol/mg pro vs. 0.40 +/- 0.63 fmol/mg pro; n = 5; P < 0.05). In summary, dopamine, acting through DA1 receptors, decreased AT1 receptor expression in proximal tubule, an effect likely mediated by increased intracellular cAMP levels. Local dopamine production also led to decreased AT1 receptor expression, suggesting dopamine may reset sensitivity of the proximal tubule to angiotensin II.

Angiotensin II upregulates type-1 angiotensin II receptors in renal proximal tubule.

Angiotensin II (Ang II) is an important regulator of proximal tubule salt and water reabsorption. Recent studies indicate that rabbit proximal tubule angiotensin II receptors are the type-1 (AT1R) subtype. We studied the effect of Ang II on proximal tubule receptor expression. Rabbits were treated with either angiotensin converting enzyme inhibitors or a low salt diet to modulate endogenous Ang II levels. In captopril-treated rabbits, liver and glomerular AT1R mRNA levels increased 242 +/- 125 and 141 +/- 60%, respectively (n = 6-7; P < 0.05), as determined by quantitative PCR. In contrast, proximal tubule AT1R mRNA levels decreased 40 +/- 11% (n = 6; P < 0.05). Binding of 125I Ang II to renal cortical basolateral membranes of captopril-treated rabbits decreased from 2.9 +/- 0.55 to 1.4 +/- 0.17 fmol/mg protein (n = 6; P < 0.025). In rabbits fed a sodium chloride-deficient diet for 4 wk, AT1R mRNA levels decreased 52 +/- 11% in liver and 43 +/- 7% in glomeruli (n = 4-5; P < 0.05), whereas they increased 141 +/- 85% (n = 5; P < 0.05) in proximal tubule. In basolateral membranes from rabbits on the sodium chloride-deficient diet, specific binding of 125I Ang II increased from 2.1 +/- 0.2 to 4.3 +/- 1.1 fmol/mg protein (n = 7; P < 0.05). To determine whether Ang II directly regulates expression of proximal tubule AT1 receptors, further studies were performed in cultured proximal tubule cells grown from microdissected S1 segments of rabbit proximal tubules and immortalized by transfection with a replication-defective SV40 vector. Incubation of these cells with Ang II (10(-11) to 10(-7) M) led to concentration-dependent increases in both AT1R mRNA levels and specific 125I Ang II binding. Pretreatment with pertussis toxin inhibited Ang II stimulation of AT1R mRNA. AT1R mRNA expression was decreased by either forskolin or a nonhydrolyzable cAMP analogue (dibutryl cAMP). Simultaneous Ang II administration overcame the inhibitory effect of forskolin but not dibutryl cAMP. These results indicate that proximal tubule AT1R expression is regulated by ambient Ang II levels, and Ang II increases AT1R mRNA at least in part by decreasing proximal tubule cAMP generation through a pertussis toxin-sensitive mechanism. Upregulation of proximal tubule AT1R by Ang II may be important in mediating enhanced proximal tubule sodium reabsorption in states of elevated systemic or intrarenal Ang II.

Induction of heparin-binding epidermal growth factor-like growth factor mRNA in rat kidney after acute injury.

Previous studies have suggested that EGF or other members of the EGF family of mitogenic proteins are involved in proliferation of renal tubular epithelial cells occurring during recovery from injury to the kidney. The present studies examined whether expression of mRNA for the recently identified heparin-binding EGF-like growth factor (HB-EGF) is regulated in response to renal injury induced by either ischemia/reperfusion or mercuric chloride. Increased expression of HB-EGF mRNA was demonstrated in the post-ischemic kidney within 45 min of unilateral ischemia/reperfusion in the rat. Induction of HB-EGF mRNA occurred only when ischemia was followed by reperfusion, and was not eliminated by removal of blood cells from the post-ischemic kidney by saline perfusion. In situ hybridization with 35S-labeled antisense riboprobes of HB-EGF indicated that compared with control, there was increased HB-EGF mRNA expression in the 6 h post-ischemic kidney in the inner cortex and outer medulla in a patchy distribution, with the greatest expression in the inner stripe of the outer medulla. Expression occurred primarily in tubular epithelial cells. Recombinant human HB-EGF stimulated [3H]-thymidine incorporation in both primary cultures of rabbit proximal tubule cells and NRK 52E normal rat kidney epithelial cells, with potency similar to that of EGF. Induction of HB-EGF mRNA was observed in tubules freshly isolated from rat renal cortex or outer medulla when the tubules were subjected to reoxygenation after incubation in anoxic conditions. The nephrotoxin, mercuric chloride, also caused induction of HB-EGF mRNA both in vivo and in isolated rat cortical tubules. The anoxia/reoxygenation-induced expression of HB-EGF mRNA in isolated tubules was inhibited by the free radical scavengers, di- and tetra-methylthiourea, indicating involvement of reactive oxygen species. These findings indicate that HB-EGF mRNA is inducible in the kidney in vivo by acute tubular injury and suggest that HB-EGF may act as an autocrine/paracrine growth factor involved in proliferation of tubular epithelial cells and repair of the kidney.

Angiotensin II attenuates renal cortical cyclooxygenase-2 expression.

We have previously shown that in rat renal cortex, cyclooxygenase-2 (COX-2) expression is localized to cTALH cells in the region of the macula densa, and that dietary salt restriction increases COX-2 expression. Administration of the angiotensin converting inhibitor, captopril, further increased COX-2 mRNA and renal cortical COX-2 immunoreactivity, with the most pronounced expression in the macula densa. Administration of an AT1 receptor antagonist, losartan, also significantly increased cortical COX-2 mRNA expression and COX-2 immunoreactivity. Mutant mice homozygous for both Agtr1a and Agtr1b null mutations (Agtr1a-/-,Agtr1b-/-) demonstrated large increases in immunoreactive COX-2 expression inthe cTALH/macula densa. To determine whether increased COX-2expression in response to ACE inhibition mediated increases in renin production, rats were treated with captopril for one week with or without the specific COX-2 inhibitor, SC58236. Plasma renin activity increased significantly in the captropril group, and this increase was significantly inhibited by simultaneous treatment with SC58236. Thus, these studies indicated that angiotensin II inhibitors augment upregulation of renal cortical COX-2 in states of volume depletion, suggesting that negative feedback by the renin-angiotensin system modulates renal cortical COX-2 expression and that COX-2 is a mediator of increased renin production in response to inhibition of angiotension II production.

Role of p38 in the regulation of renal cortical cyclooxygenase-2 expression by extracellular chloride.

We have previously shown that in renal cortex, COX-2 expression is localized to macula densa and surrounding cortical thick ascending limb of Henle (cTALH). Dietary salt restriction increases local expression of COX-2, which mediates renin production and secretion. Given that decreased luminal chloride [Cl(-)] at the level of the macula densa increases renin production and secretion, we investigated the role of extracellular ion concentration on COX-2 expression. Quiescent rabbit cTALH cells were incubated in a physiological salt solution containing high or low levels of NaCl. Immunoreactive COX-2 expression increased significantly in the low NaCl solution. COX-2 expression also increased after administration of the Na(+)/K(+)/2Cl(-) cotransport inhibitor, bumetanide. Selective substitution of chloride led to increased COX-2 expression, whereas selective substitution of sodium had no effect. The p38 MAP kinase inhibitor PD169316 decreased low NaCl-induced COX-2 expression. Low-salt or low-chloride medium induced cultured cTALH to accumulate >/= 3-fold higher levels of pp38, the activated (phosphorylated) form of p38; low-salt medium also increased pJNK and pERK levels. Feeding rats a low-salt diet for 14 days induced a significant increase in renal cortical pp38 expression, predominantly in the macula densa and cTALH. These results suggest that reduced extracellular chloride leads to increased COX-2 expression, which may be mediated by activation of a p38-dependent signaling pathway.

Oncofetal protein accompanying irradiation-induced small-bowel adenocarcinoma in the rat.

A tumor-associated protein was found in tissue derived from an X-irradiation-induced adenocarcinoma in the small bowel of the rat. The protein was associated with the cell membranes of the tumor tissue. It shared common antigenic determinants both with a rat fetal protein and a perchloric acid-soluble protein isolated from the serum of the tumor-bearing rat.

Cyclic nucleotide concentrations in 7.12-dimethylbenz[a]anthracene-induced pancreatic cancer in rats.

Pancreas cancer was induced in noninbred male Holtzman rats by the implantation of beeswax containing 7.12-dimethylbenz[a]anthracene (DMBA) into the "head" of the pancreas. The tumors that developed 4--6 months later were examined for their cyclic AMP and cyclic GMP levels. The lesions could be considered in one of two categories according to their cyclic nucleotide contents: lesions with significantly smaller amounts and those with greater amounts, compared with levels measured in the pancreas tissues of the control rats. The existence of two biochemically distinct groups may indicate different growth patterns of the DMBA-induced pancreatic neoplasia.

Identification and characterization of a circulating tumor-associated oncofetal protein from a radiation-induced adenocarcinoma of the rat small bowel.

A tumor-associated protein from the cellular membranes of a radiation-induced rat small bowel adenocarcinoma was identified, found to be serologically unaltered in the circulatory system, and was observed to be susceptible to acid hydrolysis. The immunochemical reactivity was unchanged by heat, alkali, or neuraminidase digestion. The protein appeared to be a single immunologically active species, but it was structurally composed of a heterogeneous group of proteins.

Purification and characterization of a phosphotyrosyl-protein phosphatase from wheat seedlings.

A neutral phosphatase which catalyzes the hydrolysis of p-nitrophenylphosphate has been purified to homogeneity from wheat seedlings. The enzyme is a monomeric glycoprotein exhibiting a molecular weight of 35,000, frictional ratio of 1.22, Stokes' radius of 260 nm, and sedimentation coefficient of 3.2 S. That the enzyme is a glycoprotein is surmised from its chromatographic property on Concanavalin A-Sepharose column. An examination of the substrate specificity indicates that the enzyme exhibits a preference for phosphotyrosine over a number of phosphocompounds, including p-nitrophenylphosphate and several glycolytic intermediates. Both phosphoserine and phosphothreonine are not hydrolyzed by the enzyme. The phosphatase activity is not affected by high concentrations of chelating agents and does not require metal ions. Molybdate, orthovanadate, Zn2+, and Hg2+ are all potent inhibitors of the phosphatase activity. The ability of the phosphatase to dephosphorylate protein phosphotyrosine has been investigated. [32P-Tyr]poly(Glu,Tyr)n, [32P-Tyr]alkylated bovine serum albumin, [32P-Tyr]angiotensin-I, and [32P-Tyr]band 3 (from human erythrocyte) are all substrates of the phosphatase. On the other hand, the enzyme has no activity toward protein phosphoserine and phosphothreonine. Our result further indicates that the neutral phosphatase is distinct from the wheat germ acid phosphatase. The latter enzyme is found to dephosphorylate phosphotyrosyl as well as phosphoseryl and phosphothreonyl groups in proteins. In light of the many similarities in properties to phosphotyrosyl protein phosphatases isolated from several sources, it is suggested that the wheat seedling phosphatase may participate in cellular regulation involving protein tyrosine phosphorylation.

Renal effects of non-steroidal anti-inflammatory drugs and selective cyclooxygenase-2 inhibitors.

Nonsteroidal antiinflammatory drugs (NSAID) are one of the most commonly used medications worldwide to inhibiting COX activity for the treatment of pain and inflammation. Their nephrotoxicity has been well documented. With the development and clinical implementation of new COX-2 inhibitors, the safety, including the effects on renal function and blood pressure, is attracting increasing attention. In the kidney, COX-2 is constitutively expressed and is highly regulated in response to alterations in intravascular volume. COX-2 metabolites have been implicated in mediation of renin release, regulation of sodium excretion and maintenance of renal blood flow. Similar to conventional NSAIDs, inhibition of COX-2 may cause edema and modest elevations in blood pressure in a minority of subjects. COX-2 inhibitors may also exacerbate preexisting hypertension or interfere with other antihypertensive drugs. Occasional acute renal failure has also been reported. Caution should be taken when COX-2 inhibitors are prescribed, especially in high-risk patients (including elderly and patients with volume depletion). Recently, agents with combined lipooxygenase/COX inhibition and agents that combine NSAIDs with a nitric oxide (NO) donor have been reported to reduce adverse renal effects.

Cyclooxygenase-2 inhibition decreases renin content and lowers blood pressure in a model of renovascular hypertension.

It has been proposed that the macula densa participates in the regulation of increased renin expression in renovascular hypertension (RVH) and that prostaglandins may be among the mediators of macula densa function. We have previously shown that in renal cortex, cyclooxygenase-2 (COX-2) expression is localized to the macula densa and surrounding cortical thick ascending limb and increases in high-renin states, such as salt restriction and angiotensin-converting enzyme inhibition. In the present studies, we examined the effect of the selective COX-2 inhibitor SC58236 on plasma renin activity (PRA) and renal renin expression in RVH in rats. The aorta was coarcted between right and left renal arteries, and animals received either SC58236 or vehicle for 1 week. At day 8, vehicle-treated coarcted rats were hypertensive (mean carotid arterial blood pressure: 138+/-3 versus 87+/-2 mm Hg in sham-operated controls; n=9 to 11; P<0.001) and exhibited a disparity of kidney size (ratio left/right kidney: 0.78+/-0.04 versus 1.02+/-0.02; n=9 to 10; P<0.001). PRA increased significantly (84.6+/-6.5 versus 9.0+/-1.4 ng angiotensin I [Ang I] per milliliter per hour; n=8 to 9; P<0.01). In the coarcted rats, neither renin mRNA expression nor renin activity of the right kidney was altered (renin/GAPDH mRNA: 1.12+/-0.05-fold levels in control rats; n=6; P=NS; renin activity: 23.4+/-1.8 versus 27.1+/-3.4 ng Ang I per hour per milligram protein; n=8 to 9; P=NS). However, the renin mRNA of the left kidney increased to 3.0+/-0.6-fold of control (n=6), and the renin activity increased to 189.0+/-28.6 ng Ang I per hour per milligram protein (n=8; P<0.01). Expression of COX-2 mRNA and immunoreactive protein increased in the affected left kidney but was not different from control in the unaffected right kidney. SC58236 treatment to coarcted rats did not affect kidney size (ratio left/right kidney: 0.79+/-0.06; n=9). However, PRA was significantly decreased compared with the vehicle-treated coarcted rats (19.8+/-2. 8 ng Ang I per milliliter per hour; n=9; P<0.01). The left kidney renin mRNA and renin content were also decreased (1.7+/-0.3-fold control; n=6; P<0.05; and 45.7+/-7.6 ng Ang I per hour per milligram protein; n=9; P<0.01, respectively), while renin mRNA and renin content of the right kidney were not altered. SC58236 lowered mean arterial blood pressure (122+/-5 mm Hg; n=14; P<0.05 compared with vehicle). A significant correlation was observed between PRA and mean blood pressure (r=0.75; P<0.01). In summary, these studies indicate that the selective COX-2 inhibitor SC58236 decreases renin production and release in RVH and suggest an important role for COX-2 regulation of the renin-angiotensin system.

Expression of B-type endothelin receptor gene during neural development.

Mutations of the B-type endothelin receptor (ETRB) gene have been found to cause defects in the development of enteric neurons, which resulted in aganglionic megacolon in rodents and humans. To determine the distribution of ETRB mRNA during neural development, mainly in the CNS, in situ hybridization was applied at various developmental stages of rat. ETRB gene was abundantly expressed prenatally in the ventricular and subventricular zones, as well as postnatally in the ependymal and subependymal cells. ETRB mRNA was also strongly detected prenatally in the dorsal root ganglia, as well as postnatally in the cerebellar Bergmann glial cells and epithelial cells of choroid plexus. Our data suggest that ETRB acts as a regulator in the differentiation, proliferation, or migration of neural cells during development.

Cell-mediated cytotoxicity expressed by lymphoid cells from rats with asbestos-induced peritoneal mesothelioma towards rat fetal cell.

Cell-mediated immunity (CMI) directed towards rat fetal cells was evaluated in Fischer F344 young inbred male rats having asbestos-induced peritoneal mesothelioma. The tumors were induced by exposure to Canadian chrysotile B fibers and the CMI delineated by the injury and destruction brought about to 6- to 10-day-old primary fetal cell cultures by the so-called educated peripheral blood lymphoid-cells (PBLC) obtained from the cancer-bearing rats. A significant cytotoxicity was found to be expressed by the PBLCs, suggesting that during the development of mesothelioma, a cellular retrodifferentiation occurs, thereby educating the effectors to recognize a common determinant existing in both the tumor and fetal cells. Educated PBLCs were produced from rats having endodermal tissue cancers (adenocarcinomas of the small bowel, colon and pancreas) and were found to also be cytotoxic to the fetal cultures, yet no injury was apparently inflicted upon cultured mesothelioma target cells by these effectors. These results suggested that the tumor education was specific and that probably a unique and different fetal component was being recognized by the effector cells obtained from the rats with lesions arising either in the mesodermal or endodermal tissue. Further support for this concept was the failure of an antibody, specific to an oncofetal protein existing in endodermal lesions, to apparently recognize any common oncogenic proteins in the mesothelioma. Preliminary studies have also been accomplished which suggests the existence of natural killing immune responses existing to the mesothelioma target cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Prostaglandins in macula densa function.

Cyclooxygenase (COX)-2 mRNA and immunoreactive protein localize to the macula densa and adjacent cortical thick ascending limb in renal cortex, and chronic NaCl restriction increases expression of this enzyme. These findings suggest an integral role for eicosanoids generated by macula densa-associated COX-2 in mediating renin release. As selective inhibitors of COX-2 become available, it will be important to assess their effects on the renin-angiotensin system and glomerular hemodynamics.

Post-partum antibody-dependent cell-mediated immunity in the rat following perinatal exposure to iodine-131.

A study was recently completed which indicated the first generation of adult rats that had been exposed perinatally to iodine-131 possessed peripheral blood lymphoid-cells capable of expressing cytotoxicity towards cultured small bowel adenocarcinoma target cells, i.e., active antitumor cell-mediated immunity (CMI). The results gathered during the current investigation suggest that such animals similarly express anti-tumor antibody-dependent cell-mediated immunity (ADCC). The animal model employed consisted of Fisher F344 inbred rats exposed to iodine-131 (sodium) during their 16th to 18th day of gestation, and at an interval of two months post-partum when the offsprings had matured into adults, they and their mothers were evaluated for the presence of serum components capable of expressing ADCC activities toward X-ray induced small bowel adenocarcinoma target cells. Significant ADCC activities were found to be expressed by the offspring while no analogous immunological responses could be detected in the serum of the mothers. This lack of maternal ADCC activity suggests the existence of a biological block developing during pregnancy resulting in the mother being immunological nonresponsive to carcinogenic insults. One serum component present in the offspring identified as being responsible for initiating ADCC was an immunoglobulin of the IgG class as based upon its physical characteristics: solubility, molecular weight, and reactivity with anti-immunoglobulins, pepsin, and protein A. The interpretation of these findings is that perinatal exposure to radioiodine results in the development of cells having foreign-like properties in the offspring which are recognized by the animal's immune system, thus resulting in detectable antitumor CMI and ADCC immune responses.